NSCI 175 Final (All Learning Objectives)

Describe how an action potential is propagated along an axon

Action potentials are regenerated along the axon. Each adjacent section is depolarized and a new action potential occurs.

Describe the functional differences between the dorsal stream and the ventral stream

Dorsal stream- assessing the location of objects (where) and guiding our movement toward them Ventral stream- identifying objects (what).

Define the following key anatomical reference terms: dorsal, ventral, rostral, caudal, mid-sagittal, horizontal, coronal, ipsilateral, contralateral, proximal, distal

Dorsal- towards the back Ventral- towards the front/stomach Rostral- towards the nose Caudal- toward the butt Mid-sagittal- a cut that divides the left and right. Can see the corpus callosum. Horizontal- cut that separates the dorsal and ventral. Coronal- divides brain into anterior and posterior parts Ipsilateral- on the same side of the midline Contralateral- on the opposite side of the midline Proximal- closer to body Distal- farther away from body

Describe the available treatments for anxiety disorders

Drugs that reduce anxiety are called anxiolytics Benzo's- enhance GABAA receptor function. Side effects include drowsiness, dizziness, and decreased alertness and concentration. Interferes with memory formation and consolidation; anterograde amnesia. SSRI's: can treat both anxiety and depression, which often occur together. Some can treat anxiety apart from depression.

Explain why action potentials move away from the cell body

Due to the absolute refractory period. Na inactivation gates are closed, not allowing the threshold to be hit towards the soma of the neuron. But if an action potential is generated in the middle of the axon, it can go both ways.

Describe how EPSPs and IPSPs contribute to the generation of an action potential in the post-synaptic cell (draw a diagram to illustrate this)

EPSPs depolarize the membrane towards the threshold, IPSPs polarize the membrane away from threshold.

Explain how information is organized in the olfactory bulb

Each cell detects different odorants. Clustering together. This is when it starts to get organized.

Describe how cells of the cerebral cortex are organized

Each have different layers. Can have different shapes. Granule and pyramidal cells. Parallel to surface of the brain. Layer closest to the surface is separated from the pia mater by a zone that lacks neurons (molecular layer, layer 1). At least one cell layer contains pyramidal cells that emit large dendrites, called apical dendrites that extend up to layer 1 where they form multiple branches.

Compare and contrast taste buds and papillae

Each papillae have taste buds along them. 1 papillae has many taste buds. The little things we see on our tongue are papillae. Tastebuds are located down and in. 1 taste bud has multiple taste cells. Axons come off of the back (not neurons since no soma)

Describe the difference between 'efferent' and 'afferent'

Efferent- carries information from the CNS. Exiting information. Movement Afferent- carries information to the CNS. Away from the body. Sensation.

Explain the concept of unconscious emotions

Emotion: pattern of physiological responses and species-typical behavior. In humans, responses are accompanied by "feelings". 3 components to an emotional response: 1. Behavioral- muscular movements appropriate to situation that elicits them 2. Autonomic- provide quick mobilization of energy for vigorous movement. Increase SNS and decrease PNS. 3. Hormonal- secretion of Epi and NE further increases blood flow to muscles. Controlled by separate neural systems Integration of responses is controlled by the amygdala. We are not always aware of our emotions. May feel restless without knowing what emotion is causing that feeling. Can influence behaviors and decision making without being aware of it. Humans can be primed by reading lists of positive, negative, or neutral words and shown faces. Negative words will prime people to see negative emotions in the pictures. Neutral words = neutral faces. Depending on the priming, perspective of faces look different.

Explain how pain receptors work

CMR1= cool-menthol receptor 1. Free nerve ending TRPV = transient receptor potential vanilloid TRPV1 = capsaicin receptor. Detects hot. Small, unmyelinated slow C fibers carry information from CMR1 and TRPV1 receptors signaling cool temperature or dull pain. Large, myelinated fast A delta fibers carry information from TRPV2 receptors signaling sharp pain.

Describe the gross organization of the mammalian nervous system in terms of the two divisions: the central nervous system (CNS) and the peripheral nervous system (PNS). Include a description of what each part does in terms of function

CNS: brain and spinal cord The brain consists of the cerebrum (sensation and movement), brain stem (life-sustaining functions and relays information), and cerebellum (fine movement and balance) PNS: nerves

Describe the methods used to investigate the internal structures of the brain (CT, MRI, fMRI, PET)

CT- a measure of X-ray absorption at several positions around the head, maps tissue density. Structure. MRI- provides higher resolution images. Structure PET- gives images of brain activity. Uses radioactive traces and maps their destinations by the emissions. Identifies which brain regions contribute to specific functions fMRI- detects changes in brain metabolism (oxygen use) in active brain areas. The amount of oxygen available is measured indirectly (BOLD). Can show how networks of brain structures collaborate. Function.

Describe the molecular basis of muscle contraction

Ca binds to troponin which changes conformation so that myosin heads can bind to actin, causing contraction. ATP binding to the heads causes them to detach.

Compare and contrast the lateral pathways and ventromedial pathways in terms of anatomy and function

Lateral- independent limb movements. Corticospinal tract- cortex to spinal cord. Travels down the right side and crosses over at the medulla and now on the left side in the spinal cord to control the left side of the body. If you lesion the left Corticospinal tract above the medulla, you will have trouble moving your right hand. Particularly hand and fiber movements. Also rubriospinal tract- red nucleis to spinal cord. Ventromedial- posture and trunk. Vestibulospinal tract- balance. Vestibular nucleus to spinal cord Tectospinal- tectum to spinal tract. Head and knowing where you are in space.

Summarize key neural mechanisms of sleep Discuss how the activity of modulatory systems changes with wakefulness, non-REM sleep, and REM sleep Compare the role of the sleep-promoting factors adenosine and melatonin

NE neurons- straightfoward. LC. Fire during awake and enhance arousal and wakefulness. When sleeping, NE is slowed down. Increased firing while awake. Decreased while asleep 5-HT- it's complicated. Increase firing during waking and slow during sleep. Lesion in the RN alone, causes hyperactivity and insomnia. Decreases in 5-HT results in insomnia and alterations when REM stages happen. Increase 5-HT, suppressing REM and increases sleep. See in depression. When people put on SSRI's, increase sleep at night when they were having insomnia before. More complicated. Maybe involved in sleep staging because of alterations in REM. ACh- in pons and midbrain. Some of these neurons enhancing REM. Involved in initiation in REM sleep; other ACh neurons active when awake. REM is more of wakeful state in brain. Histaminergic neurons: monoamine (same family as sero). Receptors in brain different than body. Enhances wakefulness. Antihistamines bring you to sleep (benadryl crosses BBB). Orexin- intimate connection between sleep and wakefulness (energy regulation). Same from feeding. When lost, result in narcolepsy. Narcolepsy is characterized by REM intruding on wakefulness. Important for regulating REM and keeping REM during sleep and not letting it happen during the day. Adenosine are produced during wakefulness. Breakdown product from ATP. Caffeine is adenosine antagonist. Adenosine levels lower in morning and higher later in day. Reduced while sleeping. Once threshold, you go to sleep. As people drink coffee regularly, getting adaptations so that adenosine levels get higher or more receptors. Take away caffeine, you're in withdrawal and groggy. Produced during increased neuronal activity. Occur in different amounts and brain regions. Accumulation in the VLPA of the hypo and regulates sleep. Triggers neurons in VLPA to get activated and they inhibit wakefulness systems in the brain, leading to sleep. If you destroy VLPA, causes total insomnia and is fatal in rodents. Increased during slow wave and REM sleep. Sleep promoting region provides inhibition to cortex, ACh neurons, histamine neurons, NE neurons in LC. By inhibiting these 3, result in shutting down wakefulness areas. VLPA is GABAergic. Sleep theory: sleep need- indicate how long you've been awake. Start low in morning and increase throughout day until sleep. S factor is adenosine (also others). Other factor is sleep urge (C factor). Circadian factor. Cycles to it. Goes down and up at 2 pm then down then up again. Synchronize sleep/wake cycle with day and night. Peaks in middle of night. Supposed to be asleep already. Melatonin. Troph at like 10 am. Another mini peak at 2pm (my nap is from 2 to 4 lol).

Compare and contrast the neurotransmitter-gated ion channels and G-protein-coupled receptors of each of the above systems

NT gated ion channels: very fast, shorter effects, not as selective as voltage gated ion channels.G-protein-coupled receptors: slower, longer lasting, and more diverse post synaptic actions.

Define pain. Explain why it should be viewed as a positive adaptation

Pain is the body's emergency signaling system. It's supposed to deter having damage done. If you didn't feel pain, you would have a harder time figuring out if something is wrong or dangerous.

Explain how simple and complicated tastes are represented using population coding

1 neuron doesn't represent the taste of something. Each cell has a preference, but they fire for other things too. This is population coding. Thousands of taste cells all put together will have a primary taste that the brain will understand.

Describe three ways that pain is regulated

1. Afferent regulation- Information from both touch an pain going to the spinal cord. Touch synapses onto GABA interneurons, inhibiting the pain fibers. This is why rubbing your foot when you've stepped on a lego helps. 2. Descending pain pathways. PAG to the Raphe Nuclei, to the Dorsal horn. 3. Endogenous opioids- opiate drugs and endogenous opioids, including enorphins, bind to specific receptors in the brain to reduce pain.

Sketch a brain and label the four lobes of the cerebral cortex

1. Frontal lobe 2. Parietal lobe 3. Temporal lobe 4. Occipital lobe

Describe the methods used to classify neurons

1. Number of nuerites (projections). Unipolar, bipolar, or multipolar. We usually think of the multipolar 2. Dendrites 3. Connections 4. Axon length 5. Gene

Describe the four essential steps in the scientific process with examples

1. Observation- making a hypothesis and observing results 2. Replication- replicating your previous findings 3. Interpretation- what we think it means 4. Verification- getting other people to verify that this experiment works. A single experiment doesn't prove anything; it provides support for a hypothesis or theory

Explain the cellular mechanisms for each of the five tastes. Predict how a compound would affect taste given knowledge of which taste receptor it interacts with and how it acts at that receptor

1. Salty- Na ions are transported across taste cell membranes, depolarizing the taste cell. Releases serotonin 2. Sour- acids taste sour because they release hydrogen ions (H+). H+ pump results in shutting down K channels, depolarizing the cell. 3. Sweet, bitter, and umami- all have specific G protein receptors. On a givien taste cell you cannot find both sweet and bitter. All 3 receptors are coupled to Gq, causing increases in Ca. All functioning using the same G proteins, so in general, they will be on different cells, but could be coupled with salty/sour. If they were on the same cell, they would share the same G-protein pool and we wouldn't be able to tell the difference.

Compare the two main theories of memory consolidation

1. Standard theory: Early in memory formation and retrieval, need the hippo in order to retrieve memories. It pushes info to cortex for LTM, to retrieve, has to go back through hippo to use info again. During consolidation specifically. After consolidation has happened, don't need your hippo anymore in order to retrieve it. 2. Multiple trace theory- depends on what kind of memory if you need hippo. Semantic or context free (simple facts, no story) may not need the hippo to be retrieved. Also says, episodic and contextually rich memories (story like); still need hippo to retrieve the memory. Come from patient HM. Anterograde amnesia, little of retrograde, and lot of lTM still there. Types of memories, especially retrograde: could recall semantic, but episodic were susceptible to forgetting. Provided support for multiple trace theory.

Draw a diagram to help you describe each of the steps in synaptic transmission

1. The action potential is propagated over the presynaptic membrane 2. Depolarization of the presynaptic terminal leads to influx of Ca 3. Ca causes vesicles to fuse with the presynaptic membrane and research transmitter into the cleft 4. The binding of NT to receptors i nthe postsynaptic membrane opens channels, permitting ion flow and initiating and excitatory or inhibitory postsynaptic potential 5. PSP's spread passively over dendrites and the cell body to the axon hillock 6. NT break down by enzymes, reuptake, or diffuse away. Also binding to autoreceptors to shut down release of any more NT

Define the stages of memory acquisition and memory consolidation

2 stages of memory: Period of time of acquisition (info from outside world into STM). Consolidation- STM to LTM. To get STM, get modification of brain from senses. Modification of synaptic strength; will change with time and activity that supports forming memories. Consolidated requires changes in gene expression and protein synthesis.

Describe how vesicles fuse with the membrane

A clustor of protein molecules in the vesicle membrane binds to proteins in the cell membrane, creating a fusion pore. The fusion pore widens, and the membrane of the vesicle fuses with the cell membrane. Once the NT leaves the cell, the vesicle becomes part of the membrane.

Explain how the conduction velocity of a neuron varies with axonal diameter (draw a diagram to illustrate this)

A larger axon diameter allows for less internal resistance, freeing up space for the ions to flow through. Milkshake through a small vs. large straw analogy. As axonal diameter increases, conduction velocity also increases since its less likely for the ions to exit the cell through channels Lambda is the distance from origination point when V is 37^ of original V. Rm = membrane resistance Ra = internal resistance Increasing rm increases lambda Decreasing internal resistance increases lambda

Explain the differences between agonists and antagonists

A ligand is a substance that binds to a receptor. NT's are ligands, and so are many drugs. Each receptor "recognizes" one specific NT (an endogenous ligand) Ligand binding forms a ligand-receptor complex Induces conformation change in the receptor. The change induces a chain of physiological events resulting in the opening or closing in ion channels and changes in membrane potential in the postsynaptic neuron. An agonist mimics the effects of the endogenous ligand An antagonist blocks the receptor from opening Agonists have high affinity and efficacy. Antagonists have high affinity and no efficacy.

Explain how movements are planned by the brain

A motor plan is a set of muscle commands established before the action occurs. Movement is often initiated in response to sensory input. Sensory information comes in. Ventral stream. Goes to prefrontal cortex, then premotor cortex and supplementary motor area, then primary motor cortex which sends the output to the muscles.

Describe mirror neurons in terms of when they are likely to fire

A subregion of premotor cortex contains the mirror neurons. The same neurons fire before making a movement as when observing another making that movement.

Explain why a neuron needs a resting potential

A typical neuron has well defined input and output structures The resting membrane potential is the difference between the charge of the outside of the membrane and inside of the cell when no stimulus is applied A neuron needs a resting potential so that is possible for an action potential to be generated. Ohm's law states that I=gV, so if there was no difference in charge on either side of the membrane at rest (V) then there would be no current (I) to generate an action potential.

Calculate (a) the equilbrium potential for an ion using the Nernst equation and (b) the resting membrane potential using the Goldman equation

A. The Nernst Equation is E(ion) = (61.54/z)(log [ion outside]/[ion inside]) z= ionic charge Use to find the equilibrium potential B. The Goldman Equation is Vm = 61.54 log (P(ion 1)[ion 1 outside] + P(ion 2)[ion 2 outisde} / P(ion 1)[ion 1 inside] + P(ion 2)[ion 2 inside]) The equation is only used for monovalent ions! And because Cl- is negatively charged, the numerator and denominator are flipped for that ion For log: if smaller number is on top, the number will be negative

Describe acetylcholine, glutamate, & GABA in terms of anatomy, function, receptors, and drugs targeting the systems (you do not need to memorize the specific synthesis & degradation enzymes!)

ACh: distributed from striatum for motor control, septal nucleus to hippocampus (basal forebrain) for memory storage and recall, nucleus basalis to cortex, amygdala, thalamus, and brainstem for attention, emotional memory, and REM switching. In the PNS- ventral spinal to alpha motor neurons and skeletal muscle and autonomics to smooth muscle and glands. Has nicotinic and muscarinic receptors. Drugs include nicotine, muscarine, and curare. Glu: found and projected everywhere in the brain. More point-to-point neurotransmission rather than activity in distal nuclei. Glutamate is an excitatory amino acid neurotransmitter involved in dynamic information processing activities like working memory, perception, and voluntary muscle control. Receptors include AMPA, NMDA, and Kainate; also have metabotropic as well. Drugs include MK-80, PCP, ketamine (NMDAR antagonists) GABA: found everywhere in the brain. Local inhibitory control over excitatory neurotransmission, fine balance between glu and GABA. GABAA and GABAB receptors. Drugs include alcohol, benzos, barbiturates, picrotoxin, and baclofen.

Describe the process of excitation-contraction coupling. Compare and contrast NMJ transmission with synaptic transmission between two neurons

Achetylcholine. Nicotinic receptors. NMJ: the terminal button of an efferent neuron and the membrane of the muscle fiber it synapses on. Motor end plate: the postsynaptic membrane of a NMJ. Endplate potential: PSP that occurs in the motor endplate in response to ACh release. Larger than an EPSP. Each AP induces contraction of the muscle fiber. Depolarization of the fiber opens voltage-gated Ca channels. Ca enters the cytoplasm which triggers muscle contraction. Ca is also a cofactor so that the myofiibrils can extract energy from the available ATP. Physical effects last longer than the AP. Elasticity of muscle, time required to get rid of the Ca. A rapid succession of AP's can cause a muscle fiber to produce a sustained contraction. SR has Ca. Ca induced Ca release Presynaptic looks identical The size of the post synaptic is different. EPP's definitely give AP's in a muscle cell.

Identify the characteristic(s) that all anxiety disorders share

All anxiety disorders share anxiety; what's different is what causes the anxiety (generalized, trauma, social, panic attacks, intrusive thoughts). Different than fear: anxiety is a generalized response to an unknown threat or internal conflict, whereas fear is focused on known external danger. Most anxiety manigests as feeligns of concern or worry, with responses such as increased muscle tension, restlessness, impaired concentration, sleep distrubances, and irritability. Activation of the SNS produces increased heart rate, sweating, and other signs of fight or flight response.

Draw a simple diagram to compare the pattern of neural communication between neurons of the secretory hypothalamus, network of neurons of the ANS, and diffuse modulatory systems

Almost all hormones act on more than one target organ A hormone may have different effects on each target, and act to coordinate different parts of the body. One hormone may cause a response in more than one type of receptor One target organ may respond to several hormones. 1. neuron that talks to other neurons and the other neurons go on- point to point. Restricted synaptic activation of target cells 2. Secretory hypo affect targets by releasing hormones into blood stream 3. Network of neurons of the ANS- interconnected. Work together to activate tissues all over the body 4. Diffuse modulatory systems extend their reach with widely divergent axonal projections.

Describe the placebo effect

An example of a nonspecific effect. It is a pharmacologically inert compound, but can have therapeutic and side effects. Belief in a drug may produce real phsyiological effects despite the lack of chemical activity. Expecting a medicine to works actually work via endogenous opioids getting activated.

Sketch the pain pathway from periphery to cortex

Anterolateral tract. A delta and C fibers cross at the level of the spinal cord, goes through midbrain, then thalamus, then cortex.

Describe the main types of glial cells, including the main function of each

Astrocytes- physical support, clean up debris (phagocytosis), produce chemicals, aid in controlling extracellular chemical environment, provide nourishment by taking glucose from the blood and breaking it down into lactate so that neurons can take it up and use mitochondria to make it energy (does this because it's quicker than the neuron making ATP from glucose), create the blood-brain barrier, control blood flow, surround and isolate synapses. Oligodendrocytes- provide support to axons, produce myelin sheath (not continuous, series of segments) Microglia- smallest glia cells, phagocytes that break down dead and dying neurons, immune system of the brain that protect the brain from microorganisms and is the inflammatory response to brain damage Shwann cells- provide myelination in the PNS, segment consists of a single Schwann cell, can guide regrowth in case of axon damage.

Compare the behavioral and EEG characteristics of the three functional states of the brain (awake, non-REM sleep, REM sleep) Identify the EEG rhythms during the various stages of sleep (Fig 19.16)

Asynchronized: see more stuff on bottom of first graph. Awake and REM. Everyone in class just talking. Can't hear all of the same thing at once. Irregular. Synchronized: higher amplitude and slower period. Slow wave. Non-REM. Conductor can work to synchronize. Neurons that fire together Awake: alpha, and beta and gamma. Alpha are noisy and mess; slightly higher amplitude; wave form. Beta and gamma is just noise. Can't see a wave. Beta waves are involved in awake and thinking (gamma for thinking). Fastest wave. Asynchonized. Alpha is awake and resting. Neurons still asynchonis though. Stage 1 non REM: theta rhythms. Drowsy. Drift in and out. Amplitude is getting bigger. More synchronized. Stage 2 non REM: people are asleep and don't realize it. Sleep spindles and look like spiky thing. K complexes are indicative. Start with synchonise activity. Stage 3 and 4: Often pulled together as "slow wave sleep" or deep sleep. Stage 3 is diff in amount of delta rhythms. Bigger synchronise waves. Proportion of delta rhythms to everything else. More in stage 4. Synchronized activity. The further you get in sleep, the more synchronized your neurons get. Along with REM, make up first if deprived. Super groggy if woken up. REM: rapid eye movement. If you look at EOG, eyes are rapidly moving back and forth. Paralyzed everywhere else. Story like dreams. Not that you dont dream during other dreams, just story like. Beta and gamma rhythms and theta rhythms. Brain is both drowsy and very active. Pattern: 0 hours- Progress through all stages. 1 hr- spend time in 4., then bounce to 2, then REM. About 1.5 hrs. Early, lot more of deeper sleep. As you get through, less and less deep sleep. More and more REM. Cycling through. Naturally wake up at REM.

Discuss the cause of Parkinson's disease and why it is called a basal ganglia disorder

Basal ganglia: frontal, parietal, and temporal cortex project to the striatum (caudate and putamen). Striatum projects to the GP. GP projects to the VA/VL. VA/VL to the motor cortex. Basal ganglia is "informed" of planned movements and can influence these movements via this loop. D1: striatum inhibits GPi and SNR, inhibiting the thalamus, exciting the cortex. Parkinsons is a neurological disorder characterized by muscular rigidity, slowness of movement, resting tremors, and postural instability. Caused by SN DA neurons dying. DA input to the striatum facilitates movements. The lack of DA ultimately results in an increase in the inhibitpry output of the GPi (less inhibition of the inhibitor) so there is too much inhibition of the motor cortex. The lessening of GPi inhibition on the ventralmedial system is probably responsible foe the muscular rigidity and postural instability.

Explain retinotopy

Based on the 2D mapping from the retina (but distorted). Map of our retina on visual cortex. On retina, we have a map of the world in specific locations. Project back to specific locations on the cortex. The periphery ends up in the center of the cortex.

Compare basic theories of emotion with dimensional theories of emotion

Basic emotion theories: for each individual emotion, there is a distinct brain pattern of activation that can tell what emotion is by looking at an fMRI scan. Each emotion has a signature pattern. Dimensional theories: emotions can be broken down into fundamental elements. Combined in different ways and differing amounts. Emotions correspond to brain activation along dimensions such as valance and arousal. Psychological constructionist theories- variation on dimensional theories. Includes nonemotional psychological components. Emotion an emergence consequence of combined components.

Explain why the action potential is referred to as all-or-none

Because if threshold is reached the action potential will fire every time, but if that threshold isn't reached it absolutely cannot fire

Describe the biological theories of affective disorders

Biological explanation for depression emerged from the discovery of 2 antidepressants; MOAI and NET and SERT inhibitors. Led to the monoamine hypothesis of depression. Depression is caused by insufficcient activity of monoaminergic neurons. Evidence- dperession can be caused by monoamine antagonists. Suicidal depression is related to decreased CSF levels of 5-HIAA. Tryptophan depletion procedure causes depressed patients in remission to have a relapse of depression. Problems: drugs used to treat depression don't work immediately, even though monoamines are increased immediately. Some placebo effect. If you think it'll work, helps it to work. Diathesis-Stress hypothesis: begins with the effects of stress on the brain. Interesting because this hypothesis provides an explanation as to why stress is an important mediator of depression. People with Cushing's syndrome have high levels of GC's and are prone to depression. People who have died by suicide have cortisol Hospitalized patients with depression show high levels of cortisol.

Describe what constitutes an EEG signal—which neurons, what kind of activity?

Brain electricity. When an EEG is measured. Looking at gross electrical activity of the brain. Average. Of area underneath electrode. Place on scalp. Info in the area below that (generally only cortical info, cannot get subcortical). All the info you're getting has to get filtered through the upper layers. Lose any fast signals. Cannot record AP's. Get an averaged response from neurons. Measuring synaptic waves. Looking at a bunch of EPSP's and IPSP's averaged. If ton of neurons at once, could see what looks like an AP, but that means a ton of synchronized activity.

Explain the reductionist approach

Breaking the topic of neuroscience down into smaller pieces (Cognitive, Behavior, Systems, Cellular, Molecular). Pros: can be more detailed; get a better explanation of the topics Cons: can bterm-0e hard to see the big picture

What are other functions of glia not covered well in your textbook?

Building and breaking synapses NG2 cells are in a potential stage Glia communicates both with itself and neurons through chemical means. Glia have receptors for chemical messages, and strengthen neuronal messages. Also functions in learning.

Draw a diagram to explain the process of distributed memory storage

Cell assembly process. Neural network model- unique pattern or ratio of activity of neuronal activity. Distributed memory. No single neuron represents single neuron- firing of all neurons give you the memory. Memories can survive even when damage to individual neurons. Slow degradation of memories with neuron loss. Physical change in brain; synaptic strength. Not static. Plastic. Every experience you have changes brain. Each neuron encodes different parts of memories.

Illustrate the taste responsiveness of taste cells and their gustatory axons

Cells can respond to multiple tastes, but tend to have preferences. If the cell gets depolarization, the axon will then fire more. Changes in firing rate. Axons fire spontaneous, but when there is a response, you see an increase in action potential frequency.

Sketch a brain and label: cerebrum, cerebellum, brain stem, thalamus, ventricles and spinal cord. Describe what each of these parts do in terms of function

Cerebrum- outside layer of the brain responsible for sensation (parietal lobe) and movement (frontal lobe). Cerebellum- "little brain" in the back, has it's own section. Needed for fine movement and balance Brain stem- pons, medulla, and the midbrain- tectum. Assist in motor reflexes. Has superior colliculus Thalamus- relay station for sensation and movement. Almost all information goes through. Interacts with neural circuits in the cerebral cortex Ventricles- spaces in brain filled with CSF Spinal cord- mediates the transmission of afferent and efferent neural signals between the CNS and the body

Name the major components of the olfactory epithelium and describe their functions

Cilia that detect the odorants Specific receptor cells that have their cilia in the mucus. They synapse onto axons. Basal cells Supporting cell that makes mucus for odorants to dissolve onto Bowman's gland Able to make new cells. Adult neurogenesis.

Discuss physiological and biochemical processes that vary according to a circadian rhythm

Circadian rhythmycles are daily rhythmic change in behavior or physiological processes. Internal clocks. Dark/light cycles varies. Will be maintained if you have lights on/off all time. Number of things that vary: alertness (sleep and wakefulness), temperature (increased during day and lowest night), GH highest at night while asleep. Cortisol is highest in morning right before waking up; midday increase. Help you be able to wake up. Enables you to get out of bed without passing out. Potassium is low i morning and increases throughout day. Activity rhythms: every time mouse rotates wheel once, puts black mark on paper. The more active, the more black marks. Used to have continuous record and cut each day and line up. Now have signal sent to computer to have chart. Indicates wakefulness and activity.

Describe the biological theories of schizophrenia Discuss the relationship of the mesolimbic DA system and mesocortical DA system with the symptom categories of schizophrenia Summarize the evidence that glutamate is involved in schizophrenia Describe the structural differences in the brains of people who have been diagnosed with schizophrenia vs. people who have not been diagnosed with schizophrenia Explain the age of onset in the context of the neurodevelopmental hypothesis

Classic DA hypothesis: schizophrenia results from excessive DA activity. Why DA? 1. Drugs that increase DA activity such as amphetamine, can induce psychotic symptoms in people who do not have schizophrenia and exacerbate psychotic symptoms in some schizophrenia patients at doses that do not produce psychosis in controls. 2. Drugs that effectively reduce psychotic symptoms are DA receptors antagonists, and their clinical potency is strongly correlated with their ability to block DA D2-like receptors. Thought is that people with schizophrenia have more DA release in the mesolimbic pathway (positive symptoms) and less DA release in mesocortical pathway (negative and cognitive symptoms) Role of glutamate: PCP and ketamine also induce psychosis and it resembles both the positive and negative symptoms of schizophrenia and they are antagonists at the NMDA receptors. Lower than normal densities of NMDARs in the PFC and striatum. NMDAR encephalitis has symptoms that look similar to schizophrenia. Structural differences: Ventricular enlargement: more cortical loss. Cannot be explained by loss of NMDAR's or increases in DA. Takes time to develop. Thicker corpus callosum- loss of gray matter in the frontal lobes, and less metabolic activity. Disorganized neurons. Neurodevelopmental hypothesis: Must be different stages that happen in the course of someone who goes on to develop the disorder. Early stage (first hit): genetic predisposition alters which genes expressed. In utero changes. Viruses, toxins, complications, etc. Alters how brain is structured in first place. Together, leads to early neurodevelopment changes. Nueron formation and migration, pruning, apoptosis. Chagnes in structure of brain. Latent stage (before have disorder)- supposed to be prodrome. Subtle signs. Motor abnormalities, social withdrawal, deficits in processing tasks. Will be people that go through first hit and latent stage that dont end up with schizophrenia. Late stage (2nd hit)- excessive pruning in adolescents resulting in alterations in function. Environmental insults (stress, substance use). When all together, get schizophrenia. Changes from in utero to diagnosis. When people are diagnosed in early adulthood, already had these changes in the brian.

Describe the procedure for producing learned fear

Classical conditioning. Pairing a context (NS) with an aversive stimuli like a shock (US). After conditioning, the previous NS becomes a CS and just having the context alone will elicit fear. Using US of a shock or something else with a fear response leads to increased ANS and stress homones, BP, freezing response. Pair it with a CS. By itself, the CS will elicit the fear response.

Describe the neural circuit that supports learned fear

Conditioned emotional response: produced by a neutral stimulus that has been paired with an emotion-producing stimulus. Some stimuli automatically produce fear reactions (loud unexpected noises or shocks). Shock is detected by the soma cortex. Tone is processed by the auditory cortex. Both go into the amygdala and get processed. Within the amygdala, bunch of synapses. CeN coodinates the CER, output to the hypo and PAG. Hypo regulates the hormonal response and PAG regulates the behavioral reaction. Cortex deals with the emotional experience (Feelings). If you lesion different parts of the circuit, you get different outcomes If you do training and then lesion the CeN, you lose the learned behavior. Only have behavior with the US. Leaning CeN, lesion hypo = behavioral response, but lose ANS; no increase in HR and BP or cort, but you see freezing behavior. If you lesion the PAG, you still see increases in HR and BP, but not freezing behavior.

Describe the evidence that LTP is involved in memory

Correlational observations- time course of LTP is similar to that of memory formation. Somatic intervention experiments- blocking LTP (drug that blocks NMDA) impairs learning. DAPV blocks NMDAR and impairs learning. Overexpressed NMDAR = enhanced learning. Behavioral paradigm- fear conditioning. Which side of box it can trust. Gets shock in dark side. Wait for a bit. When door opens, animal huddles in corner and wont go through door. While learning, animal had electrodes implanting- stimulating and recording. Measured baseline. Then they had animals do conditioning, when they did training, they saw LTP at the synapses; they didn't do any induction. They did behavioral task and then saw LTP. The better the animal learned, the more LTP. LTP underlies learning and memory.

Describe dopamine, norepinephrine, and serotonin in terms of anatomy, function, receptors, and drugs targeting the systems

DA: nigrostriatal path from the SN to the striatum for movement. Mesolimbic path from VTA to NAc and amygdala in reward and motivation. Mesocortical path from VTA to PFC for short term memory, planning, and problem solving. All metabotropic receptors. Drugs include cocaine, amphetamines. NE: locus coeruleus to forebrain. Needed for arousal, attention, and learning/memory. Drugs include amphetamines. 5-HT: midbrain raphe nuclei in forebrain and brainstem raphe nuclei to spinal cord. Drugs includecocaine, LSD, and SSRIs. Every one of hallucinogins is a full or partial 5-HT2A receptor agaonist.

Explain how zeitgebers impact circadian rhythms

Dark period and light period. Far more activity during dark and far less when light. Rodents are nocturnal. Light synchronizes sleep/rest area. If you switch animals to have a 24 hr dark period; still have period of wakefulness and rest. Not synchronized. Shifts and where the rest is and where wakefulness is. Not consolidated. Lost the zeitgeber (light). If we lose our dark/light cycle, our circadian rhythm will shift. Zeigtgeber synchronizes sleep and wake times.

Describe the function of each component of the neuron

Dendrites- usually many per neuron, diameter tapering progressively toward ending, no hillock-like region, no myelin sheath, often much shorter than axons Axons- usually one per neuron with many terminal branches, uniform start until start of terminal branching, has a hillock, usually covered in myelin, ranging from practically nonexistent to several meters long. Soma- where most of the metabolic activity happens Axon terminals- where neurotransmitters are released Microfiliments- skeleton draped with membrane. Not static, can change and move

Describe the medical interventions used to treat substance abuse

Detox: benzos to help ease withdrawal Replacement therapy with agonists- nicotine patch or methadone Antagonists- may produce withdrawal sympotms. Naloxone and naltrexone. Alters drug metabolsim- antabuse, gives unpleasant side effects when drinking Reward-blocking medications- blocks positive reward effects of the abused drug but may produce a lack of all pleasureable feelings Anticraving medications Immunization- prompts the immune system to remove targets drugs from circulation before reaching brain.

Describe what factors determine each neuron's unique physiology

Different neurons have different action potential firing patterns Largely due to differential expression of ion channels (properties and number)

Explain the problems with the idea that there is a single system for emotions

Difficulties with the single emotion system concept: Diversity of emotions and brain activity. Many structures are involved in emotion. There is no one-to-one relationship between structure and function. Distributed network of information going over many structures. Unlikely that different parts of the brain are active for any one emotion.

Describe the somatosensory pathway to the brain

Dorsal column -> crosses at vedulla -> VPN -> primary somatosensory cortex

Describe the functional differences between the dorsal and ventral roots of the spinal cord

Dorsal roots- sensation. Brings information from the body to the brain. Afferent Ventral- movement. Brings information from the brain to the body. Efferent.

Define homeostasis, anabolism and catabolism

Energy regulation involves shuttling of energy between stores and available energy. We have 3 areas for energy regulation: 1. Available energy- blood glucose levels; gives energy for cells to use 2. Short-term storage- liver and muscles. After you've eaten and used what you need, the rest can be shuttled away for short term storage. Can be pulled out pretty easily when you haven't eaten for a while or for exercise. Lots of shuttling. 3. Long-term storage- fat. Long term energy storage. Each fat has 1000s of kJ for energy. The brain receives sensory and environmental inputs, short-term, and long-term signals. Can lead to behavioral changes like eating or not eating. Brain will signal back to body to alter metabolism. Low long term storage may signal to slow down metabolism. Adaptive since most of humanity lived through famine. Homeostasis: implies that there is a standard set point and detection system. We want to stay within the set point ranges. The detection system must: 1. Recognize deviation from set point 2. Alter physiology or behavior to correct imbalance 3. Recognize when correction has been effective Applies well to the regulation of available/short-term energy (particularly blood glucose)--traditional ideal of homeostasis Applies in the same way to the long-term regulation of energy stores and feeding--more interaction with environmental factors (and more allostasis) Anabolism- storing energy. Building up proteins. Catabolism- using energy. Breaking down amino acids for energy.

Diagram a neuron and label its components

From left to right: dendrites, soma, axon hillock, axon and myelin sheath, axon terminals

Label these structures on a mid-sagittal (medial surface) view of the brain: four lobes of the brain, cingulate gyrus, corpus callosum, thalamus, hypothalamus, tegmentum, tectum, pons, medulla, cerebellum. Describe what each of these parts do in terms of function.

Frontal lobe- thinking, planning, and movement Parietal lobe- somatosensation Occipital lobe- sight Temporal love- hearing, language, and memory Cingulate gyrus- covers the corpus callosum. Involved in processing emotions and behavior regulation Corpus callosum- connects the cortices of the two hemispheres (information doesn't cross here though) Thalamus- relay center for sensory information Hypothalamus- king of the hormones. Below the thalamus. Endocrine epicenter. Tegmentum- above the pons. Central core of the brainstem. Includes structures like the red nucleus, substantia nigra, PAG, and VTA Tectum- behind the tegmentum. Involved in certain reflexes. Pons- Bulge in the brainstem. Involved in the control of breathing, communication between different parts of the brain, and sensations such as hearing, taste, and balance. Medulla- Needed for vital reflexes like breathing, coughing, vomiting, and sneezing. Cerebellum- needed for fine movement and balance. Corrective movements.

Describe how the HPA axis is regulated by the amygdala and the hippocampus

GC's bind to the hippo and provides negative feedback as well. Hippo shuts things down so hypo stops making CRH. Or GC's bind directly to hypo for negative feedback as well. Starts by stress coming in, activating the amygdala, activating the hypo. Effects of chronic stress on hippo and amyg: Hippo- without stress, pyramidal cells have lots of dendrites. Stress causes dendrites to shrink, shorter and fewer. Not able to be activated by as much input. Not able to process info appropriately. Dentate gyrus has neurogenesis, but with chronic stress, we see inhibition. Taking together, results in shrinking of hippo and not able to function like it once was; underfunctioning. Amyg- opposite. Basolateral neurons have dendritic hypertrophy. Overall, amyg becomes hyperactive.

Discuss the memory functions of the hippocampal system

Getting info transformed into a way for it to be stored and then retrieved. Dynamic process-always active components. Sensory info coming in, will become a memory eventually. Coming in to sensory cortices. Gets processed and encoded into working/short term memory. WM- reliant on PFC, pulling info from sensory memory; immediate memory you are working with at any given moment. STM- slightly different from WM, both involved in performance of an action and knowledge. STM to LTM, consolidation. Hippo is involved in this consolidation step. Helping STM into LTM. In order for LTM to be retrieved, they have to go back into STM, then have to be consolidated again. Loss of information. Very detailed memories right after something happened, but now not as detailed.

Describe the HPA axis in terms of structure and function

Glucocorticoid release is controlled by cells in the PVN of the hypo. PVN axons terminates in the median eminence and secrete CRH into the pituitary portal system. CRH stimulates the anterior pit to release ACTH. ACTH enters the general circulation and stimulates the adrenal cortex to release GC's, which act on target tissues.

Describe adaptation

Gradual decrease in responsiveness of a neuron when exposed to the same stimuli over time A tendency of pyramidal cells -- they cannot sustain a rapid firing rate, so the frequency tends to slow down regardless of how strong the current is.Note that stellate cells can sustain a steady firing rate

Discuss the stress response and list a few consequences of chronic stress

HPA Axis. CRH --> ACTH --> GC. GC release functions: help break down protein and convert it to glucose. Makes fats available for energy. Increase blood flow. Stimulate behavioral responsiveness. Suppresses secretion of sex hormones. Acute stress: Demands of recent past and near future. Easily recognizable and tied to events/actions. Also acute episodic. Irritability, anxiety, depression; ANS arousal Chronic stress: Unrelenting demands with no perceived end. May be physical or psychological. Breaks down immune system over time. Suicide, violence, heart attack, stroke.

Sketch a hippocampal slice and use your sketch to support an argument for studying synaptic plasticity in the hippocampus

Hebb proposed that when 2 neurons are repeatedly activated together, their connection will become stronger. Hebbian synapse- synaptic strength changes if 2 neurons fire together. If you activate the 2 synapses on bottom and no response by postsyn., you get pruning of those synapses and strengthening of the synapses that elicited a response. If post syn fires an AP, you see a strengthener of the synapses. If pre doesn't cause post to fire, see a weakening. Give rise to learning. Plasticity is any changes that occur. Determined that you can measure in hippo circuits Trisynaptic circuit.- multiple area. CA is rams horn. DG as well. First step from EC. Layer 2 cells. Perferant pathway onto DG granule cells. 2 different bundles of axons that project to different areas of dendrites of dentate gyrus. Then, DG projects to CA3 (MF is mossy fibers). Glu, so are CA3. Projects to opposite side of brain; also to the CA1 neurons. CA1 project out of hippo. Well organized circuit and where to record from. Last part not part of trisynaptic. EC layer 3 coming in and axon bundle synapses on CA1 directly (TA pathway). Far enough a part to isolate. Same thing with DG bundles. Know exactly what synapses you are recording from. DG or in CA1 (can in CA3, but different plasticity).

Describe how the reward system and rewarding properties of drugs can be studied in the laboratory

How do you determine if a rat wants something? Electrical self-stimulation. Skinner box. Lever press = reward. Rate is correlated with the value of the reward. Incentive-motivation. How motivated is an animal to seek out reward. A hungry animal often ignored available food in favor of the pleasure of stimulating itself electrically 2000 times per hour for 24 consecutive hours. You can study the reward pathways by blocking receptors in certain areas or stimulating specific areas like the NAcc to see what happens to lever pressing.

Compare how heroin, nicotine and cocaine alter dopamine signaling

Heroin: Beta-endorphin and opiate drugs increase VTA cell firing by inhibiting the inhibitory GABAcells. Effects of opioids are in the VTA as opposed to NAcc. Opioids bind to GABA cells and shuts down GABA release. Removing the inhibition from the DA neuron so it can fire more APs. Relieve inhibition from DA neurons that project to the NAcc. Nicotine: The addition of nicotine results in the activation of alpha-7 nAChRs on Glutamatergic terminals and densensitization of non-alpha-7 on GABAergic cells. Increases Glu and decrease GABA = more excitability of DA neuron. BLocking non alpha 8, losing the excitation of GABA cell, so losing inhibition. Cocaine: Most of cocaine's actions can be explained by its ability to block reuptake of 3 NT's: DA, NE, and 5_HT. These transmitters are cleared from the synaptic cleft by membrane transporters. Cocaine binds to the transporters and inhibits their function. Cocaine binds most strongly (with highest affinity) to the 5-HT transporter, followed by the DA transporter, and then the NE one. Projected to NAcc. Looking at the terminals in NAcc.

Examine how lesions of the hippocampus affect spatial memory

Hippo involved in different types of memory. Converting sensory STM into LTM. Also supports spacial memory of objects of importance. Also for storage of memories for some period of time. Removing hippo, end up not being able to convert STM to LTM; lose out on future memories and tiny bit of retrograde as well. Spatial memory: radial arm maze. Which arms will have a treat when lights are on (visual cues and textural cues). Has to learn where to find reward and % of correct responses. Control animals- % of correct responses is 75% after a few second day; goes down with longer delay. Overall, animals do well. Hippo lesion- even after only 1 second delay, only at 50% of correct responses. Far more poorly than animals that still have hippo; gets a little worse over time. Unable to even learn how to find rewards in maze. Stopped spacial memory from happening.

Summarize the significance of proper hypothalamic function and its relationship to homeostasis

Homeostasis: adaptive behavioral responses to nutrient deficiencies, metabolic imbalances, and other treats to the internal milieu in order to maintain certain critical survival variables at optimal levels. Regulatory mechanism have 4 characteristics: 1. System variable is the chraracteristic that is to be regulated: body temp, thirst, hunger. 2. A set point is the optimal value that the system variable should take. 3. Detector monitors the value of the system variable. 4. A correctional mechanism is responsible for restoring the system variable to the set point. Negative feedback is an important factor in all regulatory systems. Negative feedback is the process by which the effect produced by the action serves to diminish or terminate that action. Body temp: the system variable is temp and the set point is 98.6. The correctional mechanisms include sweating and this action through negative feedback turns off the sweating behavior. The hypothalamus is the region that controls all of this.

Describe how the resting membrane potential is maintained

Ions: Na, Cl, K, Ca. As long as the concentration gradients are maintained. Primarily by the Na/K pump, keeping K in and Na out.

Summarize three ways that the hypothalamus responds to sensory input to maintain homeostasis (i.e. humoral, visceromotor, & somatic motor)

Humoral- the hormone response. Signaling to brain about storage and body. Visceromotor- Autonomic nervous system. Changes in how the ANS responds. SNS is fight or flight and PNS is rest and digest. SNS will get energy out to use in the fight/flight response. PNS wants to get food and digest/store it for a rainy day. Somatic motor- may not even be away of. Drive to eat and go to eat something. Activity levels. If you've had enough food, you may have more energy and feel more active. Deprived leads to reduced energy.

Describe how a cell assembly could support memory

Idea about what's going on to support formation of memory and then retrieval. External events represented in cortical cells. Each sense related to given event is distributed over entire brain. Reciprocally interconnected. Simultaneously active neurons that give rise to a cell assembly. Consolidation process; type of plasticity. Fire together, wire together. Active neurons end up continuing to be active as we think about events that occurred. AP's at same time, they grow stronger and stronger connected between each other. 1 neuron will cause all other neurons in that assembly to fire as well, bringing up the memory. Spread out all over brain, more reliable. Involving neurons with sensation and perception.

Describe how a modulator can change length constant

If a potassium channel closes from the G-protein activation, the lambda increases.

Understand the relationship between the concentration inside and outside the cell represented by the equations

If the concentration on the outside of the cell is greater, then the potential will be positive. If it is greater on the inside, the potential will be negative. Basically, membrane potential will be whatever charge is needed in the cell to combat the diffusive forces. (EX: potassium diffuses out of the cell naturally, so a negative charge in the cell is needed to draw it back in to reach equilibrium).

Determine when and why a researcher would use specific methods for studying neurotransmitter systems (neurotransmitters + receptors) including immunocytochemistry (or immunohistochemistry), in situ hybridization, Cre technology, neuropharmacological analysis (agonists, antagonists, etc), and ligand binding methods.

Immunocytochemistry: Use color-tagged antibodies to target particular neurotransmitters in the brain (visible under a microscope in regions where the antibodies are localized).In Situ hybridization: chemically label the probe mRNA that codes for a certain protein or peptide (visible under a microscope where the natural mRNA and the probe bind together in certain neurons).Neuropharmacological analysis: apply a certain drug or neurotransmitter to a postsynaptic dendrite and monitor the post-synaptic response (agonists activate the receptor and antagonists bind to the receptor site but just sit there and take up the space to prevent the receptor from being activated. Cre is used to get a fluorescent protein to a specific part of the brain to light it visualize those specific neurons.

Describe the organization and function of the posterior parietal cortex

Involved in organizing visually guided movements.Sends information to the primary motor cortex. The dorsal stream. Need to know where your arms, legs, etc. are and where objects are to correctly manipulate these objects.

Compare and contrast neurotransmitter-gated ion channels and g-protein-coupled receptors

Ionotropic receptors: ligand binding = conformation change in the protein leading to the opening of the ion channel allowing ions to pass through. Relatively fast. Usually selective for a particular ion. Metabotropic receptors: more than 50 different kinds of GCPR and most NT interact with GPCR. Single protein chain that weaves in and out of the membrane 7 times. Receptor is coupled to a G-protein. Ligand binding will result in affecting an ion channel or G-protein affects an enzyme. The enzyme controls the production of a 2nd messenger. 2nd messengers travel throughout the cell and can have many affects like opening ion channels, enter the nucleus and affect gene transcription, change Ca levels. Relatively slow. Suited for slow sustained signaling or modulating fast transmission.

Predict the site of a lesion in the retinofugal pathway based upon the visual field deficit List the structures of the retinofugal pathway

Light comes in through the eye -> optic nerve -> crosses at optic chiasm -> goes to LGn -> goes to primary visual cortex If you cut the left optic tract, you would lose your whole right vision. If you cute ht right optic tract, you'd lose your whole right vision If you cut the left optic nerve, you wouldn't see the left periphery. Your left eye wouldn't see anything, but the right eye makes up for everything except the left periphery. If you cut the optic chiasm, you lose the periphery on both sides.

Identify and describe the cells of the retina and discuss the pattern of their interconnections

Light goes through pupil and gets to back of eye where we detect it. 3 layers of cells. Flipped. Light comes in and passes through ganglion and bipolar layers before photoreceptors. Bipolar and ganglion cells can't detect light itself Light is detected by photoreceptors at back of eye. Send signals to bipolar cells. Then they synapse onto ganglion cells. They naturally fire Ap's and have slow rate on own. Either increase or decrease firing rate and alters perception in brain. Axons make up the optic nerve. Horizontal cells- interface between photoreceptors and bipolar cells. Work across space. Averaging data across when need convergence Amacrine cells- interface between bipolar cell and ganglioin cell. Also convergence. Help ave4rage out data across space.

Compare and contrast wanting and liking

Liking is the mechanism of enjoying something like a drug. Positive reinforcement. Wanting is the mechanism of motivation to seek out the drug. Negative reinforcement As time goes on in addiction, people begin to like the drug less and less, but the motivation to seek it out increases. If you were to block dopamine, you would only block wanting. If you were to mimic the action of dopamine (stimulating the VTA), whatever the rat was doing at that moment becomes reinforcing, and they will do that behavior over and over again. A common brain myth is that dopamine mediates sensory pleasure. Dopamine is involved in wanting and motivation seeking Opioids are involved in liking and pleasure (and mediates dopamine as well).

Discuss the circuitry in the hypothalamus (i.e. regions, neurons, and peptides) that is important for long term regulation of feeding

Long-term storage: Adipose tissue (fat)- stored energy is tapped when the body has used up short term storage/mechanisms. Argued it world be adaptive to have fat stores. More likely to survive harsh winters, periods of famine, and to reproduce (high energy costs). More mechanisms to start eating than to stop (also advantageous). Fat stores are homeostatically maintained to have relative fixed levels. Systems interact and include redundancies. In adult animals, body weight is generally stable around a "set point" but will change with long-term changes in feeding (more likely to trend upwards than downwards); primarily due to changes in metabolism and adipose tissue. Set points can change over time! As you impose starvation, weight drops. As soon as you stop, the body weight comes back up. If you keep the starvation period for a very long time, there will be changes in metabolism to stop the body weight from decreasing and becomes very efficient. If you force feed, the body weight will increase. As you stop, weight goes down. Leptin: if your brain stops paying attention to leptin, you will have an increased appetite and gain weight. Leptin is a peptide released by adipose tissue. Receptors in the hypo (arcuate nucleus). Genetically engineered mice with two different genetic mutations either: ob/ob or db/db. Ob/ob- lack of the ability to make leptin. Since no leptin is made, there is no way for the brain to know that there is enough fat, causing the mouse to eat a lot more food and put more away as storage. Db/db- leptin insensitivity. Causes insulin resistance and diabetes 2. No matter how much fat is on the body, the brain cannot interpret the signal and thinks its starving to death. Prompting to eat and slow down metabolism. Hypothalamic control: hormones from the body drive a hypothalamic appetite controller. A circuit within the arcuate nucleus integrates peptide hormone signals from the body. Sends signals to the lateral hypothalamus, which is involved in causing us to eat, seek out food, and a slowing of metabolism. MCH and orexin neurons stimulate appetite and reduce metabolic rate. Peptide Y and AgRP neurons produce to the MCH and orexin neurons and activate them. Leptin inhibits these neurons. Alpha MSH (POMC) and CART neurons project to the MCH and orexin neurons and inhibit them. Leptin activates. Leptin says we have enough in storage and that we don't need to eat as much for a while (appetite is like climate; hunger is like weather) Increases in leptin: POMC and CART are activated, inhibiting the MCH and orexin neurons and the lateral hypothalamus; this inhibits feeding behavior. Also activates the PVN, projects to stress systems and TH release. PVN active --> ACTH release --> cortisol release. Preganglionic neurons in the SNS activated. Stress response pulls energy out of storage and uses it. Increases in metabolism and inhibits feeding. All without conscious control. Decreases in leptin: NPY and AgRP will be active, stimulating the LH and feeding. Inhibition of PVN, decreasing ACTH and TH. Not using as much energy. Store things to not lose energy.

Describe the available treatments for depression Discuss the mechanisms of action of MAOIs, TCAs, SSRIs, SNRIs and how they related to the monoamine hypothesis Compare and contrast Ketamine/Esketamine and previous pharmacological treatments (MAOIs, TCAs, SSRIs, etc.) Explain the common mechanism that the pharmacological and non-pharmacological treatments share and describe how it relates to the glucocorticoid hypothesis

MAOI's: irreversible inhibitor of the enzyme that breaks down the monoamines. Requires strict dietary restrictions to prevent potentially fatal hypertensive crises. TCA's: block reuptake of serotonin and NE. Many side effects. SSRI's: selective serotonin reuptake inhibitors SNRI's: serotonin and NE reuptake inhibitors. Ketamine/Esketamine- more emerging and not well established. Very rapid symptom relief. Side effects include hallucinations and psychotic episodes. Vagal nerve stimulation; ECT very effective for those not responsive Psychotherapy and meds are effective and moreso combined than either alone. Drugs reverse the effects of the shrinkage of the hippo. Can take 4-6 weeks for neurogenesis. Ketamine does this rapidly. Chronic stress decreases BDNF in the hippo, which then contributes to the atrophy of the CA3 neurons. Increasing NE and serotonin leads to an increase in BDNF downstream.

Describe the organization of retinal inputs to the LGN

Magnocellular- whether or not something is moving; whether or not you are seeing an object; big cells = big picture -> where Parvocellular- fine details; sensitive to color; texture' shape; depth. Figure out what the object really is. Parvo is little cell -> what.

Explain the importance of the sodium-potassium pump

Maintains the resting potential. Pumps 3 Na ions out for every 2 K ions into the cell. Requires energy. Membrane is somewhat leaky to Na and leaky to K

Describe how a sensory event is encoded in action potentials in sensory fibers

Mechanosensation. Stretch receptors that physiclly open channels. Na comes in and graded potentials add up to AP's. It is possible to have a touch sensation with no AP.

Identify pathways and areas of the brain that mediate reward

Medial forebrain bundle VTA - NAcc (mesolimbic pathway). Releasing DA in NAcc. If you block the receptors, you get less self-stimulation. DA in the NAcc is the story people tell to explain the reinforcing effects of drugs. Useful idea, but not the whole story. Da in the NAcc goes up in response to a tail pinch and during restraint stress in rats. NA release in NAcc habituates even through a drug can still be reinforcing (an animal will still perform a behavioral response to obtain the drug). DA in the NAcc is not simply a signal for "good" or "pleasure". Incentive sensitization hypothesis: incentive aspect (motivating aspect) is sensitized. Much bigger over time. That is the rewarding motivator rather than the drug itself. There are a number of pathways involved. Amygdala gets involved and interneurons (GABA), opioid peptides, cannabinoids, nicotinic ACh. Changes in these pathways underlie SUD Drug reinforcers hijack the DA system causing supraphyisiological increases in DA that are not seen with natural reinforcers.

Compare membrane resistance and internal resistance

Membrane resistance is all about the amount of holes in the membrane. Having less resistance (more holes) decreases lambda Internal resistance is all about diameter. By increasing the diameter, the internal resistance decreases, increasing lambda.

Propose at least one practical implication of reconsolidation

Memory is not accurate. Not tape recorders and don't store every little piece of information. Able to be distorted. When first happens doesn't break down with time, other events that happen before and after interfere. Might get 2 memories a little confused. Every time you bring up a memory, you have the potential to add or take away new info and put it back into storage. Reconsolidation. Returning a memory into LTM after recall. Can experience memory in therapy without as much emotional charge. Sensory systems aren't accurate; subject to perception. Depending on already formed beliefs, your experience of an event while it's happening can be very different from others. No objective truth for events. No point to storing details. All you need is gist of something so you know where to get info again. Storing info that will help us in the future. Memory and contamination and misinformation effect. Show people film clips of crashes, depending on how you word the question, that changes the estimate of how fast. "Smashed into each other" - faster. "Hit each other" - slower. "Contacted each other" - slowest. All the same car accident, just different words would be enough to see different estimates. Imagine then that depending on how you get asked, change your recall and what you report out. Not great if expects jury to believe eyewitness testimony. Never can trust completely. Prep for trials- asked over and over again, may change over time because integrating additional info as time goes on. By the testimony, could be very different. Problems with relying on memory. Practical uses: memories that are disturbing or under trauma resulting in PTSD. Exposure therapy. Reexperience the memory repeatedly, but without the trauma occurring physically. Reconsolidated as a memory less emotional than before. The act of playing tetris while rexperiencing memory reduced stress levels later on.

Explain how histological procedures contributed to the advancement of neuroscience

Microscopes and staining were used to visualize the cells. Cajal used the Golgi stain. Cajal did the drawings and drew in the gaps.

Compare different levels of analysis in neuroscience research (molecular, cellular, systems, behavioral, and cognitive neuroscience)

Molecular- looking at the molecules that bind to receptors and how that can change the receptors Cellular- how molecules work together to give neurons their special properties. How do neurons communication? What are their different functions? Different types of neurons? etc Systems- how different neural circuits analyze information, form perceptions, make decisions, and execute movement Behavioral- how do neural systems work to provide integrated behavior? Cognitive- neural mechanisms required for higher level mental activity, such as self-awareness, imagination, and memory.

Describe the symptoms of depression

Mood disorder characterized by subnormal arousal. Dysfunction of the arousal systems that mediate emotion and motivation. Melancholia, anhedonia, psychomotor retardation, fatigue, insomnia/hypersombia, guilt and worthlesssness, etc.

Explain the importance of animal research in the field of neuroscience

Most of the research in this field is on animals. Humane treatment: Animal Welfare Act and the Institutional Animal Care and Use Committee.

Compare primary sensory neurons, motor neurons, and interneurons

Motor neurons: stimulate muscles or glands Sensory neurons: respond to environmental stimuli, such as light, odor, or touch Interneurons: receive input from and send input to other neurons

Describe how feeding is regulated during the phases of short-term regulation of feeding by release of intestinal peptides, insulin, and activation of sensory and hypothalamic neurons

Negative feedback of blood glucose: If glucose goes too low: brain cells cannot function leading to unconsciousness. If glucose goes to high: damage to kidney, retina, peripheral nerves, cardiovascular system. To maintain BG, we have 2 hormones: insulin made by the pancreas, which takes glucose and converts it to glycogen for storage (it's a storage hormone). Glucagon is a use hormone; it gets energy out. When BG is high, insulin is secreted and binds to receptors, which allows cells to take up glucose to either use or store as glycogen. Signals to liver and muscles. It lowers BG levels as the glucose is absorbed by cells. When BG is low, glucagon is secreted to increase it. Diabetes: Type 1- not producing enough insulin. Immune system is attacking the beta cells. Need to make insulin. No amount of diet will cause these cells to come back. Need insulin replacement therapy or pumps. Type 2- insulin receptors stop responding, becoming insensitive to the ligand. If insulin is released, it goes to bind to cells, but it doesn't work. Can't get glucose transported for energy or storage, so you end up with a higher BG. Treatment include drugs that sensitize the receptors and a lower sugar diet. Over time, if not managed, a person with type 2 will get type 1. Short-term energy balance: presence or absence of food in the gut--is reported by hormones from digestive organs. Ghrelin- appetite stimulant. Synthesized and released by endocrine cells of the stomach; reaches high levels before eating and drops off after eating. It has been shown that the brain can become insensitive to ghrelin in anorexia. Stomach releases a lot of ghrelin, so the brain becomes less sensitive. This leads to problems in refeeding. Can be difficult to start eating more food again because they aren't hungry even though the body is starved. CCK- appetite suppressant. Released by intestinal cells; reaches high levels after eating, especially after eating fatty foods. Appetite signals converge at the NST. CCK is a peptide released by the gut after feeding and acts on the vagus nerve to inhibit appetite.

Describe the available treatments for schizophrenia Compare and contrast typical and atypical neuroleptic drugs Identify which neurotransmitter receptor subtypes are the common targets of drugs used to treat psychosis

Neuroleptic- brain sleep. First developing drugs to treat positive symptoms- major tranquilizer. Typical- chloropromazine; thorazine; haldol. Older drugs interact with D2 receptor. Y axis is drug affinity from low to high. How much affinity does drug have for types. Focus on D2, 5-HT2, muscarinic ACh. Moderate to high affinity for D2; also for 5-HT2; adrenergic; muscarinic. Main thing that jumps out: all 4, antagonists of D2. Block positive symptoms. Side effects are adrenergic and muscarinic. Related to muscles, dry mouth, eyes, negative symptoms. Reduces motivation and movement by binding to D2. Parkinsonian effects. Atypical- May notice. mid-high of 5-HT2 blocking. 5HT2A activation happens with hallucinogens. Blocking hallucinations would block receptor. Newer drugs aren't interacting with D2 as much. Don't fully support DA hypothesis. Still lots of data that DA is involved. Treating DA still alleviates symptoms.

Distinguish between receptive field center and receptive field surround.

Neurons at different levels of the visual system have very different receptive fields The receptive fields of retinal ganglion cells are concentric-a circular central area with a ring around it, the surround Both bipolar and ganglion cells have 2 types: on-center/off surround & off-center/on surround The center and its surround are always antagonistic.

Explain the purpose of synaptic integration

Neurons perform information processing to integrate synaptic inputs A postsynaptic neuron will fire an action potential if a depolarization that exceeds threshold reaches its axon hillock Since postsynaptic potentials are small, synaptic integration allows them to be combined to have a significant effect on the postsynaptic neuron. Can either be spatial or temporal.

Draw the pathway that olfactory information takes, from receptor to primary olfactory cortex. Identify other regions of the brain that receive olfactory information. Compare and contrast similarities and differences between gustatory and olfactory transduction

Olfactory receptors -> olfactory bulb -> 3 connections; 1. hypothalamus -> involved in survival. 2. amygdala-> fear and emotions. 3. primary olfactory cortex. Amygdala and primary -> hypothalamus and Medial dorsal thalamus -> orbitofrontal cortex (secondary olfactory cortex) Hypothalamus -> lateral posterior orbitofrontal cortex. Goes directly to primary cortex. Very fast. That's when you have information consciously.

Describe the opioid peptides in terms of anatomy, function, receptors and drugs targeting the systems

Opiod drugs are narcotic analgesics; they reduce pain without producing unconsciousness. They create a sense of relaxation and sleep, and at high doses, can lead to coma and death. They are the best painkillers known and also produce a sense of euphoria. Produced in pituitary and adrenal glands. There are high densities of opioid receptors in the striatum, medial thalamus, locus coeruleus, PAG, and raphe nuclei. Neuropeptide precursors are made in the cell soma and transported to the presynaptic terminal. Neuropeptides are energetically expensive to make and are present in low concentrations. Endorphins are peptides that could bind to opioid receptors. Four large propeptides are processed into smaller active opioids: prodynorphin, POMC, proenkaphalin, pronociceptin.

Describe the organization of circuits in the ANS (i.e. locations of sympathetic and parasympathetic preganglionic & postganglionic neurons and their neurotransmitters)

PNS: CNS preganglionic neuron (long) release ACH onto the parasympathetic ganglion. The ganglionic neuron (short) goes to the target organ and release ACh. Muscarinic receptors SNS: CNS preganglionic neuron (short) releases ACh onto the ganglionic neuron. The ganglionic neuron (long) releases NE onto the target organ.

Compare and contrast the role of the sympathetic and parasympathetic nervous systems

PNS: Insulin release. Rest and digest. Target organs- same organs. Opposite affects. Constrict pupils. SNS: increased HR, BP, pupils dilate. Hormone releases. Glucagon. Fight or flight. Target organs- eyes, relaxing airways, heartbeat, glucose release We need both symptoms to function well. If over activation of SNS, may have problems digesting food and look like chronic stress. We do need storage and resting. Overactivation of PNS, freezing behavior. So stressed that everything collapses. No longer releasing cortisol. SNS tone to keep blood flowing.

Explain what kind of information is carried by the cranial nerves (general)

Part of the periphery. Can carry sensory and motor information. I- olfactory smell II- optic nerve II, IV, VI- muscles that move the eyes V- trigeminal, face, sinuses, and teeth VII- facial; tongue and soft palate VIII- vestibulochlear IX- glossopharyngeal X- vagus; information from internal organs XI- spinal accessory; neck muscles XII- hypoglossal- tongue muscles 12 pairs. Arise from the brain stem and innervate mostly the head. Mostly need to know X.

Understand what is meant by permeability in the Goldman equation

Permeability in the Goldman equation refers to how easy it is for a certain ion to cross the neuronal membrane. High permeability means it crosses easily, low permeability means it does not cross easily.NOTE that the potential will be closer to the higher permeability value.

Describe the serotonergic regulation of anger and aggression

Serotonin deficiency hypothesis: aggression is inversely related to serotonergic activity. Serotonergic raphe neurons project to the hypo and limbic structure via the medial forebrain bundle. Less turnover == more aggression in rodents. PCPA blocks serotonin synthesis, increases aggression In humans- resorts of the negative correlation. Sometimes aggression is treated with SSRI's.

Use a diagram to illustrate the properties of place cells

Place cells have a preference of firing. Where in space the animal is when the neuron is firing. Place field from one cell is the area where the neuron fires the most. Taking together all the place cells, could figure out where the animal is. Some cells fire in multiple places, some fire with head orientation (head direction cells). Some are time keeping track of time. Depending where, different cells fired. Put together a map and retrace rats steps based on which cells fired the most in each of the different areas. Multiple place cells and play out as animal moves. Grid cells: place cells indicares where animal is in space. Located in red. . Grid cells in enterhinal cortex (MEA). Project to place cells within the hippocampus. Instead of only firing when in one specific spot in space. If put in same enclosure and instead recorded from MEA, fire Aps in multiple different areas of the enclosure. Looks like a grid. Because of how they project and how integration works, able to take info from grid cells (multiple grid cells per place cell) results in the place field for that cell. Place field is not due to hippo, has to do with info coming in. Info from EC from sensory information.

Define LTP and discuss the properties and mechanisms of LTP in CA1 Compare and contrast input specificity and cooperativity Understand the difference between induction mechanisms and expression mechanisms

Plasticity can be measured in hippo circuits. Long term potentiation. Hours to days and enhanced effectiveness of synapses. If you can induce stimulation, can give proposed plasticity change. Electrodes into hippo into DG. Stimulating electrode on perferant path axons and recording electrode in dendrite layer. Apply stimulus that was very strong (tetanus). 100 pulses per second. Releasing NT as much as can. Recording from post syn dendrites. Recording in dendrites and stimulating once every 30 seconds so you don't induce anything. Baseline conditions. EPSPs. Then the tetanus. Could separate out 2 different pathways and tell whether or not applied tetanus or didn't to a set of synapses. Don't apply- dont see much happen. Tetanus- increase in EPSPs. Then again and further increase, and again and again. 200% of baseline. Past 24 hrs. Used tetanus to make fire at same time repeatedly then looked at difference between control. Characteristic of LTP: 1. Specificity- only get LTP at synapses where tetanus induction. Wont get where didn't provide tetanus. 2. Cooperation- unlikely to get LTP from just one synapses. Activation of many synapses at once to get LTP. Only activating 1 synapse may not be enough. Induction phase: tetanus. Inducing EPSP increase. NMDAR. Presyn terminal releasing glu and activates AMPAR. Tetanus causes massive release of glu to activate bunch of AMPAR. Depolarizing the dendrite. Kick Mg out so NMDAR opens. Coincidence detection. Ca inside cell, adding AMPAR. Relieve Mg block to allow NMDAR to get activated. Expression of LTP: normal synaptic transmission- not enough depolarization for NMDAR. Little EPSP from AMPAR response. Then induction with NMDAR activation with Ca phosphorylate AMPAR and insert more. Bigger EPSPs. Wouldnt need as much tetanus to activate NMDAR since more AMPAR. Expression relies on Ca to increase AMPAR in number and function.

Describe the symptoms of schizophrenia and classify them into their different categories

Positive symptoms: hallucinations (mostly auditory); delusions of grandeur, persecution, etc; disordered thought processes; bizarre behaviors Negative symptoms: social withdrawal; flat affect (blunted emotional responses); anhedonia (loss of pleasurable feelings); reduced motivation and poor concentration; alogia (reduced speech output); catatonia (reduced movement) Cognitive symptoms: difficulty paying attention, difficulty planning, difficulty completing tasks, memory problems

Summarize the role of the hypothalamus in aggression by citing key experimental breakthroughs

Predatory aggression- attack. Against different species for food. Few vocalizations, attack head or neck. No activity in SNS of ANS. Affective aggression- for show. Used for show, not to kill for food. High levels of SNS activity. Makes vocalizations, threatening posture. If you lesion the AMY, you get less agression. The hypothalamus and aggression: removal of the cerebral hemispheres but not the hypothalamus-sham rage. Nothign that the animal should rage about, but still a huge amount of rage. The behavior is reversed with additional lesions to the hypo. Thought to be due to the removal of cortical inhibition of the hypo. Flynn's research: elicited affective aggression by stimulating the medial hypo. Stimulated predatory aggression by stimulating the lateral hypothalamus (makes sense, since this part is known for food seeking). Two hypo pathways to brain stem involving ANS function: 1. Medial forebrain bundle --> VTA; predatory. 2. Dorsal longitudinal fasciculus --> PAG; affective aggression.

Discuss how dopamine neurons are involved in reward prediction using experimental evidence (Fig 16.17)

Prediction errors: VTA DA response is associated with sensory cues. DA response predicts reward. Incentive learning. The drive is to correct the error. A difference what we predict a reward might be and the actual reward and how that gets coded. VTA fires in response to cues previously coupled with rewards. Provides info about whether we are about to get a reward. Usual- firing after prediction and regular firing during reward. No error. Prediction with no reward: firing after prediction and NO firing during the time the reward should have been there. This is the error that we strive to correct. This may influence cravings and seeking when we haven't been able to get the drug. Cravings now trigger the same "high" feelings in established users as original drug experience. Can never recapture the original "high" by the actual drug again. The cues induce an increase in DA; a craving. Triggering the high. The cravings themselves are triggering the high, and not necessarily the drug experience.

Describe the organization and function of primary, secondary, and association cortex

Primary cortex- initiates the movement or sensation feeling. Direct processing of primary sensory or motor info. Performs the actual task of the region. Association cortex- the planning. The details. plans & integrates info for the primary area. Allows us to analyze, recognize and act on sensory input with respect to past experiences. Adjacent to primary areas and is involved in more complex processing.

Describe the organization and function of the motor cortex

Primary motor cortex is on the precentral gyrus in the frontal corteex. Stimulation of the motor cortex produces movement of the body. Somatotopic organization and motor homunculus. Big head, hands, jaw, fingers, and toes.

Describe the components of the motor control hierarchy in terms of anatomy and function

Primary motor cortex- sending output to muscles. Direct input down to motor neurons. Nonprimary motor cortex- the actual planning out of movement. Step before you actually execute. Basal ganglia- initiation of movement. Motor control loop and voluntary movement. Need info from other parts of the brain to "decide" to initiate. Suppression of unwanted movement. Cerebellum- coordination and tiny refinements in movement. Smoothly and accurately. Refining movement. Balance and coordination in general. Thalamus- interpreting sensory information. Feedback to motor areas. Also getting information from other areas about whether or not to initiate movement. Brainstem- needed for different antagonistic differences (MLR). Muscle of face, head, and neck. Spinal cord- sends out the motor neurons .Execution and reflexive control.

Design an experiment to define the chemotopic map for odorants in the brain.

Receptive fields. Maps in brain where information is organized. Maps are located in primary sensory cortices (primary olfactory cortex). Record from neurons in brain and then present odorant and see if there are increased firing rate. Then do throughout the olfactory cortex to create the map. Chemotopic maps are not location based. Not mapping out where on the tongue. Stimuli are diffusely presented to all of the cells. Organized for chemical type.

Draw a typical action potential. Label the axes and each phase of the action potential

Resting Depolarizing to threshold Rising to peak Overshoot Undershoot Refractory

Describe the experimental evidence that supports the SCN as a biological clock

Retinohypothalamis pathway- some ganglion cells in retina that project directly to hypo (SCN). Located above optic chiasm. Biological clock for mammals. Both a ganglion cell and photoreceptor (not rod or cone and not projected to by them). Has melanopsin excited by light. Resets circadian clock. Projects to other parts of hypo and midbrain and uses GABA. Taking in info about levels of light outside, going into brain and reset clock based on the light/dark cycle. Evidence it's bio clock: if you lesion, disrupts circadian rhythms under dim light conditions. Endogenous rhythm disappears. During light period, rodents sleeping and dark they are active. Lesion SCN, the rhythm and light/dark cycle start shifting around. Some sort of rhythm, but doesn't match up with the light/dark cycle. Phase shift. Dim light: is no cycle, notice that very quickly, no real consolidation of anything. No rhythm. If you have SCN intact, you still have the rhythm, just shifted. Additional evidence with brain transplants: SCN contains clock. Show that endogenous period is generated in SCN. If you lesion it and get a tissue transplant from hamster with a short period, animals take on period from animals that were transplanted with. Switching to new period. Restoration of circ rhythms, but will match the donor's period. Within SCN, molecular clocks. Similar for all organisms pretty much. Genes are turned on at certain time and turned off. Code for certain proteins present during wakefulness/sleep. Goes along with circadian rhythm.

Compare the similarities and differences between cones and rods. Explain why our vision is much better at the fovea than elsewhere

Rods nad cones correspond to 2 systmes Rods: scotopic system- high sensitivity to light. Will get active in low light. Detect low levels of light. More active in dark room. In bright light, they will all be activated and won't detect changes. High convergence. For 10 rods, 4 bipolar cells, onto only 1 ganglion cell. In periphery. Black to white. Cones: photopic system (cones). Not activated until higher levels of light. Low convergence. For every cone, 1 bipolar cell with 1 ganglion cell. Neuron in brain for that 1 cone. In fovea. Color vision. Distance from fovea: in center of eye, likely to be cones. If in periphery, likely to be rods.

Identify and describe four sensory receptors in the skin

Ruffini corpuscles- respond to indententation of the skin (deep) Pacinian corpuscles- detect mechanical stimulation and rapid vibrations Meissner's corpuscles- detect low frequency vibrations. Closer to surface. Used with two-point. Merkel's discs- respond to indentation of the skin (superficial). Closer to surface. Labeled lines- the brain recognizes distinct senses because action potentials travel along separate nerve tracts. Different receptors bring in different information.

Describe the five basic tastes

Salt- water balance. Alter water retention. Adaptive to crave. Sweet- quick energy and calories. Adaptive Umami- meat, protein, longterm energy. Amino acids used to make into own proteins. Sour- acid. Usually don't desire. Avoid. At low concentrations can be good, but at high concentrations gives tissue damage Bitter- poison. -Also evidence for detecting fat

Compare and contrast: rapidly-adapting and slowly-adapting receptors

Sensory adaptation- the neuron fires rapidly when the stimulus is first applied, but then it adapts, either slowly or fast. Tonic receptors- slowly adapting receptors that respond for the duration of the stimulus Phasic receptors- rapidly adapt to a constant stimulus and turn off. Only tells you when the stimulus is first present. Gets rid of unimportant information.

Design an experiment to find the receptive field of a ganglion cell

Shine light on the photoreceptor and see if the ganglion cell fires or not. If it fires, then it is on-center. If it doesn't fire, then it is off-center. What causes ganglion cell to fire with different stimuli.

Compare the mechanisms and circuitry involved in short and long-term regulation of feeding

Short term: Insulin and Glucagon for BG. Ghrelin stimulates appetite. CCK inhibits appetite. Both converge onto the NTS. Long term: leptin! Leptin inhibits appetite, increases metabolism, and promotes weight loss. Leptin activates the POMC and CART neurons, inhibiting the LH and feeding. If there is no leptin, NPY and AgRP neurons are active, stimulating the LH and feeding.

Describe how the human brain is similar and different from other mammalian brains

Similar structures. All have brainstems/spinal cords, and a bigger and smaller area for the cerebellum. Size is pretty proportional to the animal size. Humans have more ridges and folds for more surface area. Also have more neurons and are more complex.

Describe the hierarchy of receptive fields in the visual system

Simple cells project onto complex cells.

Explain the characteristics of receptive fields in the striate cortex Describe the main differences between simple and complex cortical cells

Simple cortical cells- bar/edge detectors-respond to an edge or bar of a particular width, orientation, and location Complex cortical cells- also respond to a bar of a particular width and orientation, but it's also moving in a particular direction.

Describe each of the components of the somatic motor system

Skeletal muscles are connected to bones at each end and fastened to muscles by tendons. Flexion- movement that tend to bend joints Extension- movement that tends to straighten joints. Lifting foot off the group is a flexion movement. Putting it down on the ground is extension. Extrafusal muscle fiber- responsible for muscle contraction. Innervated by alpha motor neurons. Single alpha motor neuron can innervate several muscle fibers. Ratio varies on the precision of the muscle movement. Muscles with precise movements such as fibers have a much lower ratio of alpha motor neurons to muscle fibers innervated. Motor unit- alpha motor neuron, axon, and the associated extrafusal muscle fibers it innervates. Intrafusal muscle fibers (make up the muscle spindle_ are specialized sensory organs. Arranged in parallel to extrafusal muscle fibers in order to detect muscle length. Gamma motor neuron- contracts the intrafusal muscle fiber. Does not contribute much to force of muscle contraction. It modifies the sensitivity of the fibers ending to stretch. If a muscle is stretched, the muscle spindle also stretches and triggers AP's in afferent sensory nerves. This triggers afferent nerve impulses to inform the spinal cord and brain of the stretch. Golgi tendons- monitor the force of muscle contractions. Detect overloads on muscles and cause a reflexive relaxing of the muscle, preventing damage.

Discuss reasons why we sleep and the consequences of sleep deprivation

Sleep is restorative. Flushes build-up in CSF. Learning and memory consolidation. Sleep deprivation- irritable, groggy, heart palpitations, hallucinations and delusions.

Compare and contrast the role of the somatic and autonomic nervous systems

Somatic PNS: innervates the skin, joints, and skeletal muscles. Voluntary muscle contraction. Cell body's axon extends all the way to the muscle. Autonomic PNS: innervates smooth muscle, cardiac muscle, and gland cells. Involuntary functions. Cell bodies start in the CNS (preganglion), and the synapse onto postganglionic cells either far away (SNS) or close (PNS) to the target organs.

Describe the organization of the primary somatosensory cortex

Somatotopy. The humonculus. A distorted form of our body. Places on our body that need lots of sensory information take up more real estate. The hands, lips, and fingers take up a lot of space.

Diagram the knee jerk reflex.

Spinal cord has some degree of autonomy. Particular stimuli can elicit rapid response via neural connections in the spinal cord. Monosynaptic stretch reflex: reflex in which a muscle contracts in response to being quickly stretched. Control of posture, correction for weight added to a muscle, and the knee jerk. Knee jerk reflex- the muscle stretches, an afferent neuron synapses goes through the dorsal root, synapses on an alpha motor neuron, goes through the ventral root and acts on the extrafusal muscle fiber.

Diagram signal transduction in an olfactory receptor neuron. Formulate a hypothesis for why the genetics of the olfactory receptor proteins are important for odorant detection.

Taking odorant molecule, binding to receptor. Turns through G protein steps into membrane potential. Molecule binds to G protein. Golf. Also find in brain as well, stimulatory type. Will activate adenylyl cyclase. cAMP will go off and will go to Na/Ca channel. Ca will activate Cl channels leading to Cl leaving the cell, depolarizing the cell. Also Ca/Na exchanger The cilia measures receptor potential. Similar to EPSP. Graded. Will depend on odorant concentration. Translated to AP firing rate. Higher concentration increases firing rate. Already smelling before thalamus.

Explain how smells are represented using population coding and temporal coding

Temporal coding- Also time code dealing with breathing (temporal). More AP than inhale than an exhale. Coding smell as stronger then. Neurons spontaneously fire. 2nd order neurons are detecting smell in first place .Third order integrates the information. Increased firing rates gets concentrated in the middle of the inhalation cycle. 3rd order neurons look at where there is the most alignment from the sums of the 2nd order. Population coding- back to idea that different neurons have different information about cells. Preference. Not that each have completely different odorants. Citrus contains multiple odorants.

Describe the effects of amygdala stimulation and lesions of the amygdala

The amygdala is involved in emotions, particularly negative (fear). Lots of nuclei. Info input coming into the lateral nucleus. Goes to medial or basal (parvocellular division), that info goes to the central nucleus. Integrating in the CeN. The amygdala talks to other areas. Bidirectional connections with many other areas. BS, hypo, PFC, thalamus, and hippo. Sensory cortex just sending input to the amygdala, no info out of it. Hypo and BS involved in the emotional response. The hypo sends out the humoral response. BS has behavioral responses. Recognition of emotion: importance of amygdala in recognizing emotional facial expressions. PET studies show amygdala activation when people are shown pictures of people expressing fear. Amygdala activation associated with BPD- AMY activity is increased regardless of expression; trouble identifying neutral faces or found them threatening. Implicates AMY in BPD. Lesions: CeN is important for the expression of emotional responses produced by aversive stimuli. Presentation of threatening stimuli cause increases in neural activity in the CeN and c-Fos expression. Lesions- animals that do not show a fear response when presented with stimuli that have been paired with aversive events. They are more tame, have reduced blood levels of stress hormones, and less likely to develop ulcers. Stimulation: CeN stimulation animals show physiological and behavioral signs of fear and agitation. Amygdala in humans: people with amygdala damage- have decreased emotional responses to fearful stimuli. Impaired acquisition of a learned fear. Impaired startle response. Have a problem with emotional memories. No increase in memory for emotionally laden stores. Have trouble recognizing emotion in facial expressions. More trouble with negative emotions (anger/fear) than with positive emotions (happiness).

Explain the Neuron Doctrine

The brain is composed of independent cells. Information is transmitted from cell to cell across synapses. Every neuron is a separate cell, not continuous with one another.

Describe post-synaptic potentials

The change in membrane local potential from the NT binding. The potential on the postsynaptic side from neurotransmitters Can be excitatory (influx of Na) Can be inhibitory (influx of Cl or efflux of K)

Explain the dendritic length constant (draw a diagram to illustrate this)

The dendritic length constant is lambda. Lambda is the distance from the origination point when the response reaches 37% of the original response size (arbitrary number). A bigger lambda means an IPSP/EPSP will retain its size for a longer distance

Explain the concept of driving force and calculate the driving force for an ion

The driving force is dependent on two things: The membrane potential at that moment (Vm) and the Equilibrium Potential (Veq) for that ion Vdf = Vm - Veq If Veq is very different from Vm, then there will be a strong driving force. Sodium's DF is an example at rest If Veq is similar to Vm, then there won't really be much of a driving force. Potassium's DF is an example at rest

Identify structures of the limbic lobe

The limbic system is involved in emotion, learning, and memory. Cluster involved in same functions. Work together as a system for learning, memory, and emotions, and how they are wrapped together. Hippocampus- rams horn shape; learning and memory. Amygdala- "almond" at the rostral end of the temporal lobe, involved in emotion, fear, and specific types of learning and memory. Fornix- fiber tract that connects the hippocampus with the mammillary bodies Mammillary bodies- protrusion on the base of the brain under the hypothalamus. Cingulate gyrus- region of limbic cortex above the corpus callosum Septum pellucidum and septal nuclei- involved in reward and reinforcement Nucleus accumbens- reward, pleasure, aggression, impulsivity.

Describe the factors that enable saltatory conduction to occur

The myelination of an axon allows for the action potential to "leap" from node to node by drastically increasing membrane resistance. Basically, the myelin separates the charges that are usually attracted to each other through the membrane (like magnets). It gives enough space so that the ions can flow through more easily.

Explain what Golgi and Cajal disagreed about

The neuron doctrine vs. the reticular theory Whether neuronal communication is continuous or not. Interconnected set of tubes (Golgi) or separate cells that communicate extracellularly (Cajal)

Compare and contrast hypothalamic control of and hormone release from the posterior and anterior pituitary. Explain which lobe of the pituitary is an endocrine gland Compare the actions of hormones released from the posterior and anterior pituitary (oxytocin, vasopressin, FSH, LH, TSH, ACTH, GH, prolactin)

The posterior pituitary is an extension of the hypothalamus. Pituitary function is controlled by the hypo. Neurosecretory cells- specialized neurons in the hypo that secrete hormones that stimulate the ant pit to release hormones. Anterior- secretes hormones that control the endocrine glands in the body. Acts as an endocrine gland. Posterior- extension of the hypo. Hypo produces hormones that get secreted by the posterior. Hormones: driven by various releasing hormones from the hypo. The ant pit secretes at least 6 different tropic hormones. Probably all of these tropic hormones and the glands they control affect behavior in some way. 2 of these hormones regulate the function of the adrenal cortex and the thyroid gland 1. ACTH- controls the production and release of hormones of the adrenal cortex. THe AC in turn releases steroid hormones. The levels of ACTH and adrenal steroids show a marked daily rhythm as they play a role in stress response 2. Thyroid-stimulating hormone (TSH)- increases the release of thyroid hormones from the thyroid gland and markedly affects thyroid gland size. 3. Follicle-stimulating hormone (FSH) gets its name from its actions in the ovary, where it stimulates the growth and maturation of egg-containing follicles and the secretion of estrogens from the follicles. In males, FSH governs sperm production. 4. Luteinizing hormone (LH) stimulates the follicles of the ovary to rupture, release their eggs, and form into structures called corpora lutea (singular corpus luteum) that secrete the sex steroid hormone progesterone. In males, LH stimulates the testes to produce testosterone. 5. Prolactin is so named because it promotes lactation in female mammals. But prolactin has a number of roles in addition to its actions on breast tissue. For example, it is closely involved in the parental behavior of a wide variety of vertebrate species. 6. Growth hormone (GH; also known as somatotropin or somatotropic hormone) acts throughout the body to influence the growth of cells and tissues by affecting protein metabolism. GH is released almost exclusively during sleep. Posterior: oxytocin and vasopressin

Describe the unconventional neurotransmitters, endocannabinoids, in terms of anatomy, function, receptors, and drugs targeting the systems

The psychoactive compound is THC. Marijuana is the most commonly available psychoactive drug originating from the serrated leaves of the cannabis plant. [THC] = 1-6% CB1 receptor distribution: hippocampus, substantia nigra, and globus palliduc. And cerebellum. Highest density in parts of the brain that influence pleasure, memory, thinking, concentration, sensory, and time perception, and coordinated movement. Endocannabinoids: AEA and 2-AG. They are retrograde messengers that carry information in the opposite direction from normal. They reduce the opening of Ca channels, reducing NT release.

Why is it difficult to determine the ratio of neurons to glia?

The ratios vary among different regions of the brain.

Summarize and illustrate the steps in phototransduction

The response of rods to light. Dark: Photoreceptors are active in the dark. Depolarized and release NT in dark (glutamate). Na channels kept open all the time. Na channels. Cyclic GMP is attached keeping it open. Rhodopsin molecules are inactive. G protein for light. So cell is depolarized and glutamate is released. Light: hyperpolarized and stop releasing glutamate. When light hits rhodopsin, it is bleached and no longer responsive to light. Results in getting rid of cyclic GMP, so Na channels close. Glutamate release is reduced. Light = hyperpolarization. How much is directly related to the intensity of light. Dim light produces less hyperpolarization than bright light. Reducing amount of glutamate, some bipolar cells are depolarized and some are hyperpolarized? Different receptors! mGlu receptors that are inhibitory when activated. Result in open of K channels and hyperpolarize. So if you reduce the amount of glutamate release, that will depolarize the cell (on-center). Turned on by having light hit the photoreceptors. Reduction in glutamate from photoreceptor, reduces amount of inhibtion on on-center. Cause on-center ganglion cell to increase Ionotropic receptor: reduce amount of glutamate causes inhibition. Off-center bipolar cell. Turned off by presentation of light from photoreceptor. More expected.

Detail the ways in which neurons are specialized for communication

The same DNA is in every cell. A cell's function is determined by the genes expressed and the way the resulting proteins are processed and packaged Synapses! Presynatpic terminals and postsynaptic membranes

Compare and contrast spatial summation and temporal summation

The sum together Spatial summation- the summing of potentials that come from different parts of the cell. Different places on the neuron at the same time Temporal summation- the summing of potentials that arrive at the axon hillock at different times. The closer together in time that they arrive, the greater the summation and possibility of an action potential. Rapid fire action potentials in one place.

Describe how demyelination affects action potential conduction

There are no Na channels underneath the myelin, so demyelination means that the action potential has to travel far on its own and can die out before it reaches the next node, getting rid of the action potential.

Explain what it means if K+ ions are at equilibrium

There is a net flow of 0 ions in or out of the membrane. Doesn't mean there is no movement of ions across the membrane, however. Rate of diffusion = electrostatic force

Compare and contrast: retinotopy and somatotopy

They are both representated based on location. The somatotopy has parts that are overrepresented based on body part. Both are spatially based and a little distorted. Organization of the maps.

Describe the functional properties of the sodium channel

They open with little delay They stay open for about one msec and then inactivate They cannot be opened again by depolarization until the membrane potential returns to threshold so that the inactivation gates can begin to open again

Explain how local anesthetics work

They temporarily block action potentials in axons by binding to the voltage gated sodium channels which prevents the axon from depolarizing.SMALL AXONS are more sensitive to being blocked and need to be excited more. As these are responsible for pain, the lack of sodium makes it harder for them to be activated.

Describe the key ionic events that underlie each phase: Threshold; Rising phase; Peak; Falling phase; Afterhyperpolarization; Refractory period

Threshold is where the action potential becomes all or nothing. Where it starts. Rising phase is because of the influx of sodium Peak is because of the closing of the sodium inactivation gates Falling phase is because of the efflux of potassium Undershoot is due to too much potassium leaving Refractory periods: absolute is when no action potential can happen due to the sodium inactivation gates being close and relative is when it takes a stronger stimulus than usual to start another action potential

Identify the criteria used to determine if a substance in the brain is a neurotransmitter and be able to determine if a substance is a neurotransmitter based on these criteria

To be a neurotransmitter, a chemical must: 1. Be produced within a neuron, and present in the presynaptic terminal 2. Be released during depolarization 3. Act on receptors to cause a biological effect 4. Have a mechanism to terminate the effect

Draw the pathway that gustatory information takes, from receptor to primary gustatory cortex

Tongue receptors -> facial, vagus, glossopharyngeal nerves -> gustatory nucleus (in the brainstem, NTS) -> VPM in the thalamus -> primary gustatory cortex NTS takes all the information from the separate areas of the tongue and consolidates it into one big message for the VPM.

Compare and contrast: pain receptors and touch receptors and their pathways

Touch: A alpha- largest in diameter and most myelinated. Proprioceptors of skeletal muscle A beta- mechanoreceptors in the skin Medial lemniscal pathway. Goes up the dorsal column and crosses at the level of the medulla, goes to VPN, then cortex. Pain: A delta- pain and temperature, myelinated. First pain C- temperature, pain, itch. Second pain. Anterolateral tract. Crosses at the level of the spinal cord, goes through midbrain, then thalamus, then corex.

Describe the difference between a "tract" and a "nucleus", using examples

Tracts- bundles of fasiculated axons in the central nervous system that are gathered into compact structures and typically share a common origin and termination; more or less analogous with nerves in the periphery. Pathways with axons. White matter Nucleus- collection of nerve cells in the brain and spinal cord that are anatomically discrete, and which typically serve a particular function. Cell bodies. Grey matter

Imagine that you want to reduce how many action potentials a given neuron can fire - propose a way to do this

V = IR V = membrane potential I = current R = resistance of the membrane Decrease the resistance of the membrane (or increase the internal resistance)

Glia either out number or equal the number of neurons in the brain, yet neurons are the predominant focus of neuroscience textbooks. Explain why that might be the case.

We focus on neurons because we could only see neuronal communication in the beginning. Glia is mostly used for support of the neurons

Illustrate and explain how human sleep patterns change with age

We sleep less as we get older, specifically REM. Very early in life- LOT of REM sleep (and in general; 16 hrs). Over time this changes. As you age, spend more and more time awake. More non REM than REM. Adult years- awake quite a bit, not much REM. More of our sleep is nREM. Old age- getting VERY little REM and little nREM. Early morning wakings. Waking up at 3-4 every morning. More and more early morning wakings. Mammals sleep more in infancy than adulthood. Infant sleep is characterized by shorter sleep cycles. Scattered with wake time; seems random early on. Around 9 weeks, see some sort of consolidation, but not all at the same time; angled. Shifts in sleep wake. Commonly seem in adults when you lose the signal of light of day vs night time. Around 16 weeks, see consolidation of awake during day and sleep at night. Elderly: lot more interruptions in sleep. Woken up in middle of night. Might be awake for quite a while. Harder time falling to sleep, maybe not even getting to stage 4 sleep. Reduction in stage 3. Very disruptive. Waking up more in morning.

Describe how the dopamine reward system changes with chronic drug use

What happens to DA after chronic drug use? In a normal control brain, there is a high density of D2 receptors in the striatum. In an abuser, there is a lot less red, suggesting fewer D2 receptors even at baseline. Placebo is the raclopride that binds to D2. Ritalin in the normal control decreases red, showing that it's fighting with the raclopride for binding, and now there will be more DA release. NOt much difference in abuse in placebo and MP. Suggesting no change in DA. No increase in DA. May not be as rewarded by natural rewards either. Don't cause increases in DA anymore. Not causing use. Sensitization of drug "wanting" but not drug "liking". DA is important for the incentive salience quality of rewards. Incentive sensitization- there is a difference between drug liking (euphoria) and drug wanting (craving). As drug addiction develops, the user experiences an increase in "watning" the drug, even though there is no change or decrease in drug liking. Berridge and Kringelbach argue that the "liking" system is focused on restricted hedonic hot spots, but the wanting system is more widespread circuit that includes the mesolimbic DA pathway.

Draw a diagram of the tripartite synapse and label its components

When an astrocyte wraps itself around a synapse to help support it. Have receptors that give a calcium rise and release substances.

Describe what happens to the membrane potential when the brain is deprived of oxygen

Without oxygen, mitochondria can't make the ATP used to power the sodium-potassium pump so the cell can't maintain a membrane potential

Differentiate when to use the Nernst and Goldman equations

You use the Nernst equation when you want the equilibrium potential for just 1 ion You use the Goldman equation to find the resting membrane potential because it takes into account multiple ions