BIOPSYCH 30 FINAL

4. Define sleep and describe the stages of sleep. Evaluate the hypothesis that sleep is a restorative Process.

Brains really active (especially hippocampus in REM) indicating that we process different things during sleep, LTM consolidation • Spaces between neurons and synapse grow larger when we don't sleep, indicated physical gunk building in brain, in sleep spaces decrease, and brain is getting rid of gunk • No sleep leads to severe cognitive impairments, attention problems, hallucinations • Sleep immunity. Body doesn't have time to recover, all systems burnt out • Newborn infants spend the most time in REM sleep, kids because brain is changing need lots of REM sleep • NREM stage 3 and 4 delta wave • NREM declines as people get older, more time in lighter phases stage ½, REM not as much as when younger • Sleep keep us safe: prevents some animals from being active during parts of day least safe from predators • Restores our bodies. NREM especially, helps restore bodies and conserve energy. • Sleep deprivation results in negative physical consequences such as reduced immune system function, can't heal, inhibition of adult neurogenesis in hippocampus • GH released in stage 3 and 4 NREM childhood helps physical growth but later in life builds muscle and bone mass and maintaining immune system function, explains why adults have more aches and pains • Memories consolidated during sleep, REM helps remember emotional material • Reorganize existing memory systems to accommodate new info, day's memories can be reactivated during NREM and redistributed to hippocampal circuits to cerebral cortex, then can be strengthened in REM easier to recall memory in waking * Sleep: is a behavior, and it is a resting state and a state of altered consciousness with a particular brain wave activity STAGES with Delta waves - slow wave sleep = stage 3,4 *Go from awake, stage 1,2,3,4, REM, 4, 3, 2, REM. Stages of sleep: Awake • Beta waves: A brain waveform 14 to 30 cycles per second, associated with high levels of alertness during wakefulness. Is characterized by highly desynchronized ( independent action of individual neurons), rapid, irregular, low - amplitude waves. Alert, active information processing, • Alpha waves: A brain waveform having 8 to 13 cycles per second, associated with less alertness and more relaxation than beta activity during wakefulness. Alpha waves are slightly slower, larger, and more regular than beta waves. Awake but resting or watching tv or meditating, trance like brain wave activity, occurs when people are relaxed. • Theta waves: A brain waveform having 4 to 7 cycles per second found primarily in early stages of NREM sleep. In children and young adults, brief moments of theta waves, organized and sustained theta waves during waking usually in cases of brain damage or neurological disorder. Theta activity characterizes lighter stages of sleep, but can begin to intrude in waking sleep deprived individuals Stage 1 NREM Sleep starts HERE!* Heart rate and muscle tension begin to decrease. Some theta wave activity now occurs 10-15 minutes Can be disturbed by muscle jerk that occurs in early stages of sleep Stage 2 NREM Occurs after 10 to 15 minutes 50% of the night's entire sleep Heart rate decreases more and muscle tension occur • Sleep spindles: Short bursts of 12 to 14 cycle per second waves last about half a second generated by thalamus/cortex interactions. Prominent in stage 2 NREM but occur in other stages of NREM. observed during NREM sleep. • K - complexes: A brief burst of brain activity consisting of single delta waves during stage 2 NREM sleep. They occur spontaneously, but also occur in response to unexpected stimuli such as loud noises. • Sleep spindles and K-complexes may reflect brains effort to keep us asleep while continuing to monitor the external environment. 15 minutes. Stage 3 and 4 NREM Occurs after 15 minutes of stage 2 Body temperature, breathing, blood pressure, and heart rate are at very low levels due to the activity of the parasympathetic nervous system. • Delta waves: A brain waveform having 1 to 4 cycles per second that occurs during stage 3 and 4 of NREM. It is the largest, slowest, most synchronized waveform of sleeping state. Difference between stage 3 and 4: • Greater proportion of stage 4 (about half) consists of delta waves. Awakening from stage 4 is more difficult and disorienting. REM • Paradoxical sleep: The first period of REM sleep happens after 90 minutes of NREM sleep. It reflects its combination of brain activity resembling waking with the external appearance of deep sleep. Transition from stage 4 to REM is abrupt, but involves usually brief passages of stage 2 and stage 3. Activity is very similar to beta activity in waking, occasional periods of theta. Vivid dreaming occurs Activity are very similar to beta waves during the wakening stage with occasional periods of theta waves as well. Eye make periodic back - and forth movements. The movements may signify the scanning of visual images during dreaming The sympathetic nervous system becomes very active. Heart rate, blood pressure, and breathing become rapid or irregular. At the same time, major postural muscles are completely inactive, effectively paralyzing the sleeper. Some smaller muscles, such as those in the fingers, retain the capacity to jerk or twitch during REM sleep. First four hours of 8 longer NREM short REM, stage 3 and 4 dominant, REM principle stage in hours 5 through 8 NREM if occurs remains in stages 1 and 2 lighter stages, last four hours stages 3 and 4 usually very little or absent Last half hour in REM

Engram Hebb synapse LTP Short & long term memory

Engram — physical memory trace in brain. The exact location has not been found. Hebb synapse — synapses strengthened by simultaneous activity • strengthening/weakening of existing synapses due to experience > strengthened when pre/postsynaptic neurons simultaneously active > weakened when pre/postsynaptic neuron activity X synchronized. • Cells that "fire together, wire together" Long-term potentiation (LTP) — type of synaptic plasticity where application of rapid series of electrical shocks to input pathway ↑ postsynaptic potentials recorded in target neurons. Short-term memory — intermediate memory store, limited amts data can be held for limited amount time; wo further processing information permanently lost Long-term memory — memory store, unlimited amts data held for unlimited amt time • Ex. Older ppl remember events that happened in childhood

Endorphins Set point Osmotic thirst Hypovolemic thirst POA Leptin

Endorphins — naturally occuring neuropeptide, related to opiates Set-point — value that's defended by reg systems (I.e. core temp, a particular body weight, fluid levels) • Deviation of ideal state assessed by the NV, makes adjustments & motivates behavior to get back to ideal state Osmotic thirst — thirst produced by cellular dehydration; lose water, balances through osmosis • Caused by Eating & digesting salty foods: more Na+ in blood makes it hypertonic relative to intercellular fluid (also coffee & exercise) • Osmotic pressure moves water out of cell to get back to isotonic (balanced) state. • Receptors sense low water volume in cells => makes you feel thirsty • Osmoreceptors — detects cellular dehydration (in brain) & alters firing rate when intercellular fluid levels change • Organum Vasculosum of the Lamina Terminalis (OVLT) — area around 3rd ventricle of brain that detects cellular dehydration > Blood brain barrier is weak here so easy to detect blood solute levels > surrounding fluid hypertonic (water in cell moves out) = OVLT firing rate ↑ (drives thirst) > surrounding fluid hypotonic (water moves into cell) = OVLT firing rate ↓ Hypovolemic thirst: thirst caused by ↓ volume of extracellular fluid; lose water & Na+ • ↓ volume interstitial fluid, blood, or both • Baroreceptors — located in kidneys & heart, senses low blood volume & measures blood pressure • Kidneys contain blood-flow receptors that respond to blood volume changes • Low blood volume → thirst initiated → kidneys act to conserve remaining fluid POA (preoptic area) — temperature: part of hypothalamus, involved in a reg functions 1. Warm sensitive neurons: 30% POA, receives input from skin & spinal cord thermoreceptors • Receptors in membrane: responds directly to changes in brain temp & blood in vicinity • Output to paraventricular Nucleus (PVN) & lateral nucleus of hypothalamus, which initiates parasympathetic activity to dissipate heat (sweat) 2. Cold sensitive neurons: 5% POA, larger amts in hypothalamus, receives input from skin & spinal cord thermoreceptors • Receives inhibitory input from warm sensitive neurons • ↓ warm sensitive neurons activity = ↓ inhibition = ↑ cold neuron activity • Output to PVN & posterior hypothalamus, activates sympathetic NV to generate & conserve heat (raises metabolism & blood vessel constriction) 3. Temp sensitive neurons: 60% POA, located in posterior hypothalamus • Steady firing rate under all temps • Input = baseline of activity in cold sensitive neurons, modified by amt of inhibition by warm sensitive neurons Leptin — substance secreted by fat cells that help the body regulate its fat stores • Fat stores low = circulating leptin low • Leptin & insulin comm w neurons in arcuate nucleus (cluster of neurons involved w feeding, located in hypothalamus) • Leptin & insulin levels low: arcuate nucleus cells release NPY & AgRP > Neuropeptide Y (NPY) — peptide NC secreted by arcuate Nucleus, initiates eating > Agouti-related protein (AgRP) — small protein secreted by arcuate Nucleus that initiates eating > NPY & AgRP communicates w LH & PVN ~ lateral hypothalamus (LH) — ~Paraventricular Nucleus (PVN) — portion of hypothalamus involved in reg of hunger • Food deprivation: NPY buildup in arcuate nucleus > NPY applied directly to hypothalamus = feeding > NPY receptors in hypothalamus blocked = fail to eat • AgRP is antagonist to MC4 receptors > MC4 receptors blocked = feeding initiated • NPY & AgRP released in LH & PVN releases TSH & ACTH > Thyroid-stimulating hormone (TSH) — pituitary hormone, stimulates growth & function of thyroid gland, ↑ metabolic rate > Adrenocorticotropic hormone (ACTH) — pituitary hormone, stimulates adrenal glands •TSH & ACTH ↑ metabolic rate, suppressing them slows body's energy use • fat stores return to normal => NPY & AgRP less active & feeding tapers off • Orexin — peptide neurochemical produced in LH, stimulates eating > Injection of orexins in hypothalamus ↑ eating > NPY & orexin levels high after food deprivation > Orexin releasing cells are influenced by leptin levels > High leptin levels = sufficient fat stored, orexin cells inhibited, feeding reduced > Low leptin levels = fat stores low, orexin cells active, feeding stimulated

Meninges Ventricles Medulla Cerebellum Substantial nigra Hypo/thalamus

Meninges — layers of membranes that cover CNS & PNS • Dura Mater — outermost, thick • Arachnoid Layer — middle (only CNS), blood vessels run through > Subarachnoid Space — spaces filled w cerebrospinal fluid (CSF), lies between arachnoid & pia mater • Pia Mater — innermost layer, overlies outer brain Ventricles — 1 of 4 hollow spaces in brain, contains CSF. Medulla — most primitive vital functions just for survival, most caudal part of hindbrain • Controls ANS responses (heart rate, breathing) • portion of brainstem, below pons & above spinal cord. Cerebellum — coordinates fine muscle movement, balance, affected by alcohol Substantia nigra — midbrain nuclei that comm w basal ganglia of forebrain • caudate, putamen, and globus pallidus Hypothalamus — part of diencephalon, participates in reg of hunger, thirst, sexual behavior and aggression, fighting, fleeing, feeding and fornicating; controls pituitary gland, part of the limbic system Thalamus — relay center for cortex & sensory info; handles incoming & outgoing signals • processes sensory info, contributes to states of arousal, participates in learning & memory

Mind-body dualism Dualism & Monism

Mind-body dualism — Descartes; body is mechanistic, mind is separate & nonphysical Monism — mind is result of brain activity Dualism — mind part of non-physical world while brain is part of the physical world, they are separate; mind can exist wo brain

PTSD Schizophrenia MDD Bipolar Disorder Anxiety GAD OCD ASD ADHD

PTSD — arises in response an extremely stressful event, intrusive memories, recurrent dreams, avoidance of stimuli associated w stressful event, heightened arousal Schizophrenia — effects ability to think, feel & behave clearly; hallucinations, delusions, cognitive impairment, mood disturbance, and social withdrawal. • Delusion — false belief/opinion strongly held in spite of conclusive, contradictory evidence • Positive symptoms — abnormal behavior (hallucination/delusion) that X occur in healthy ppl but occurs in people w schizophrenia. • Negative symptoms — normal & expected behavior that's absent due to schizophrenia (lack of motivation, asociality, apathy) • Chlorpromazine- A commonly prescribed dopamine antagonist, also known as thorazine. Major depressive disorders (MDD) — intense feelings of sadness, hopelessness, worthlessness persist min 2 weeks; due to stress, prenatal factors • Monomaimes affect it • Treat with CBT, meds, ECT > ECT Electroconvulsive therapy — treatment for depression, convulsions produced by passage of electric current through brain. Bipolar disorder — associated with episodes of mood swings, featuring at least one lifetime episode of mania, which is often preceded/followed by period of depression. • Mania — unrealistically elevated expansive/irritable mood accompanied by unusually high levels of goal directed behavior/energy that lasts abt 1 week (manic-depressive disorder) • Related to oxidative stress, imbalance in production free radicals & body's defenses against them, may lead to apoptosis Anxiety — GABA agonists, benzodiazepines • Alcohol disables prefrontal cortex, and motor function off • Share anxiety, a strong negative emotion arising from the anticipation of danger • Disrupted HPA axis, amygdala, frontal lobe inactivity Generalized Anxiety Disorder (GAD) — Severe, ongoing anxiety, interferes w daily activities. OCD (Obsessive-Compulsive Disorder) — repetitive, intrusive thoughts & need to engage in certain behaviors to control anxiety. Tardive dyskinesia — chronic disorder; involuntary, jerky movements; result of long-term treatment with antipsychotic medications. Autism Spectrum Disorder (ASD) — lifetime disorder; impairments in social interactions, & comm & range of interests • Causes: unknown > Genes that reg brain development i.e. CNTNAP2 gene (in cerebellum, impacts language) > Complications surrounding birth, SSRIs during/before pregnancy, maternal immune system abnormal responses (maternal antibodies target fetal brain protein) • Brain structure & function: brain development abnormally accelerated (brain enlargement) then period of deceleration > Microcolumns more closer together & Enlarged right hippocampus > Dysfunction in mirror system: deals w empathy, imitation, & language • Treatment: intensive, early childhood learning experiences during most of waking hours > Antipsychotic drugs, side effects: sedation & weight gain, & Antidepressants Attention Deficit Hyperactivity Disorder (ADHD) — disorder first diagnosed in childhood; inattention, hyperactivity, or both. • 2x likely in males, females exhibit inattention wo impulsivity/hyperactivity • Difficult to diagnose bc criteria involves normal behavior: symptoms must "interfere w/reduce quality of social/academic/occupational functioning" • Causes: heritability ~70+%, multiple genes involved > Brain structures affected rich in dopaminergic neurons (basal ganglia, prefrontal cortex) > env factors: lead contamination, low birth weight, prenatal exposure to tobacco/alcohol/drugs • Brain structure & function: frontal lobes/prefrontal areas: abnormal development causes delay in peak cortical thickness > Smaller volume of caudate nucleus (in basal ganglia) ~ ADHD w hyperactivity: problem in basal ganglia ~ ADHD w hyperactivity: problem in prefrontal cortex • Treatment: medication/behavioral therapy, Stimulants, methylphenidate (Ritalin), dextroamphetamine, amphetamine salts (adderall) > Amphetamines = DA & norepinephrine reuptake inhibitors → increases NT release > Methylphenidate = DA reuptake inhibitor ~ Shows that: ADHD associated w low DA activities ~ Side effects: appetite loss, sleep disturbances > Nonstimulant drugs I.e. atomoxetine = norepinephrine reuptake inhibitor

Agnosia Unilateral neglect Split brain

Agnosia — inability to recognize objects • Inability to interpret sensations so Crecognize things, typically as a result of brain damage Unilateral neglect — patients fail to be aware of items to one side of space • see it but ignore it & don't acknowledge left side of world > neglect in right parietal lobe = neglect in left world > Damage to somatosensory cortex impairs sensation & movement. • Asomatognosia — type of unilateral neglect > unaware of own left body part Due to damage to right parietal lobe Split brain — treatment for seizure disorder, commissures linking cerebral hemispheres severed • reduce seizures. • ever corpus callosum that connects hemispheres

Agonist & antagonist ACh Monoamine Amino Acids Adenosine NTs

Agonist — ↑ NC activity Antagonist — ↓ NC activity ACh — small mol NT used at neuromuscular junction in ANS & CNS • choline (diet) + acetyl coenzyme A (precursors) • AChE — breaks down ACh Monoamine — group of biogenic amine NT (DA, epinephrine, norepinephrine, serotonin) • Catecholamines — DA, epinephrine, norepinephrine > DA: Tyrosine → LDOPA →DA > Epinephrine: PNS, adrenaline > Norepinephrine: CNS, noradrenaline • Indoleamines — serotonin, melatonin > Serotonin: Tryptophan (precursor) → 5HTP → Serotonin • MAO — enzyme that breaks down monoamines, Antagonist Amino Acids — essential component of protein • GABA — major inhibitory NT of CNS, interacts w many drugs > Glutamate → GABA → glycine > Glutamate — major excitatory NT of CNS Adenosine — byproduct of ATP, Inhibitory NT NT — chemical messenger that communicates across synapse. • Serotonin — reg of mood, sleep, aggression, social status, and appetite • DA — implicated in motor control, reward, and psychosis. • Glutamate — major excitatory amino acid NT • GABA — major inhibitory amino acid NC • ACh — • Norepinephrine • Epinephrine • Glycine — inhibitory effects in spinal cord & excitatory effects w NMDA glutamate receptor. • Adenosine — byproduct of ATP, inhibitory NT

Axon Axon Hillock Dendrite Terminal button Synapse Myelin

Axon — carries signals to other neurons Axon hillock — generates AP Dendrite — receives info from other neurons Terminal button: vesicles containing NTs Synapse — junction between 2 neurons where info is transferred Myelin — insulating sheath around nerve fibers, increases the speed of impulse conduction

Classical conditioning Nonassociative learning

Classical conditioning: — type of associative learning, neutral stimulus acquires ability to signal occurrence of second stimulus • Conditioned Stimulus (CS) Sound • Unconditioned Stimulus (UCS) food • Condition Response (CR) Elicit Salivation • Unconditioned Response (UCR) Salivation Non-associative learning — type of learning that involves change in magnitude of responses to stimuli rather than formation of connections between elements/events 1. Habituation — response to stimulus continually REDUCED due to repeated exposure. • Occurs in body I.e. response to drugs over time 2. Sensitization — response to stimulus is continually INCREASED due to repeated exposure • Occurs in brain I.e. adapting to cold/hot water

7. Describe the lateralization of emotion in the cerebral cortex.

Cortical damage in frontal lobes, emotional disturbance occurs, reduced emotional feelings, especially fear and anxiety. Remove frontal lobe in chimpanzees, much calmer. Frontal lobotomies caused decrease in anxiety, but seizures, impulsivity, lack of initiative emerged Left hemisphere activity correlated with positive emotions, right hemisphere activity is correlated with negative emotions, View positive emotional stimuli, increased activation in left hemisphere , view negative stimuli correlated with activation of the right hemisphere Patients with damage to left hemisphere often depressed, right hemisphere damage cheerful Anesthesia of left hemisphere feel depressed, right side happiness. For many, the right hemisphere plays a greater role than the left in processing emotions. Right hemisphere processes emotional facial expressions faster and more accurately than the left right handed people Dichotic listening, different info is presented to each ear, info presented to left ear is processed more rapidly by right hemisphere, info presented to right ear is processed more rapidly by the left hemisphere. Sentences presented with different emotional tones to each ear, participants did better at recognizing meaning of sentence when asked to pay attent to input in right ear, more successful at identifying emotional tone when attending to left ear Meaningfulness of language is localized to left hemisphere (right ear advantage) and emotional aspects of language are processed in right hemisphere (left ear advantage) Asymmetry and facial expressions, right and left facial nerves are independent. High levels of control, including the cerebral cortex, to influence intensity of emotions expressed on the right and left halves of face. The left side of face (controlled by right hemisphere) is more expressive than right side (controlled by left hemisphere) especially in lower ⅔ of the face receives input from the contralateral hemisphere only. Bridges two hemispheres of the brain Lateralization: Right brain read emotion better, makes left side of face more expressive, and can focus and read left side better, people depressed look down to the left Right size more active you ARE more depressed. Make left active to feel better

Describe the major divisions of the brain (e.g., 3-segmented and 5-segmented brain).

Fore-brain, Mid-brain, Hind-brain (3 segments) 1. Hindbrain — brainstem, reg most basic functions: breathing, motor coordination & balance, medulla (reg breathing), most primitive functions 2. Midbrain: Tectum & Tegmentum, tracking with superior and inferior colliculi (superior = vision) (inferior= auditory tracking), substantia nigra (movement, Parkinson's pathology) 3. Fore-brain: Higher functioning, 4 lobes, hypo/thalamus 5 segmented brain • Hindbrain divides into (1) MYELENCEPHALON (medulla) (2) METENCEPHALON (pons, cerebellum) > Pons = sleep reg > Cerebellum = motor, balance, drinking affects coordination, some higher functioning (music) • Midbrain ((3) MESENCPHALON) > Tectum (above midbrain) & Tegmentum (below) > Canal between 3rd and 4th ventricle connects them and has CSF ----> cerebral aqueduct > Periaqueductal grey also found in midbrain (opiate receptors are located her for pain modulation) • Forebrain > (4) TELENCEPHALON (contains two hemispheres, cerebral cortex, frontal, parietal etc.) > (5) DIENCEPHALON (structures: hypothalamus, thalamus, basal ganglia)

Glia, neuroglia, glial cells

Glia — cells in NV, support activities of neurons 1. Microglia — phagocytosis (eat debris) & brain immune function 2. Astrocytes — help w structure, physical support, remove debris if neurons damaged make scar 3. Oligodendroglia — provide physical support & form myelin sheath around axons in brain, produces myelin in CNS 4. Schwann Cells: form myelin for PNS axons, cells can regenerate (transplants with arms can be done) Neuroglia — "glue"; provide physical support, control nutrient flow, & phagocytosis Glial cells — myelination & conduction speed, blood-brain barrier (prevent things entering brain), help neurons form new connections w eo, provides glucose for cells

8. What is the neuroendocrine stress response? In other words, describe the response of the HPA axis to a frightening stimulus. Does stress affect memory? How so?

H P A = hypothalamus, anterior pituitary, and adrenal cortex, know that amygdala turn on, cortisol feeds back to hippocampus to turn off ***The feedback for the HPA does involve feedback to the hypothalamus, pituitary and hippocampus. The primary negative feedback loop we have talked about is to the hippocampus, and an insensitivity develops with chronic feedback to the hypothalamus and pituitary. The think I told them that I want them to know is the feedback to hippocampus, and this was underscored in class. Neuroendocrine - hormone response to stress HPA axis is circuit for glucocorticoids.... Cortisol. *EXAM: Neuroendocrine stress response, HPA (hypothalamus, pituitary, adrenal) = crh , acth, cortisol feeds to hippocampus mostly and others A little DA surge with stress people may love it ****neuroendocrine stress response = the hypothalamic-pituitary-adrenal (HPA) axis mediates the stress response 1.sensory information about threat reaches the amygdala 2.amygdala sends signals to hypothalamus via stria terminalis 3. Paraventricular nucleus of the hypothalamus releases CRH 4. Anterior pituitary releases CRH 5. ACTH causes adrenal glands to release cortisol 6. Cortisol reaches neurons in brain causing increasing release of NT's 7. Hippocampus has receptor sites for cortisol, acts to inhibit excessive release of CRH. HPA RESPONSE: Neuroendocrine stress response she is referring to Some perception goes to amygdala 1. Amygdala -------> + activates hypothalamus (SEE board pic!) 2. Hypothalamus release hormone ----> CRH (or CRF) 3. CRF + activates and Goes down to anterior pituitary and causes it to release ACTH. 4. ACTH goes to adrenal gland (kidneys) causes cortisol!!!! (glucocorticoid also type) released Stressor is gone, cortisol feedback to hippocampus and hippocampus shuts everything else off CRH release hypothalamus and other hormones not released (negative feedback) Primarily goes back to hippocampus to shut everything off. Doesn't individual go back to feedback to hypothalamus and shuts it off, feed to pituitary shuts off, feed back to hippocampus which also shuts it off ) Pictures (2)!!! Sometimes tries to shut but after a while no longer can, when feeds back to hippocampus bc starts killing hippocampus, which starts dying off, it can't turn anything off anymore, other structures hypothalamus and pituitary don't respond Runaway cortisol hpa response kills hippocampus bad for health Regenerate hippocampus lots of ways strengthen grow it If it goes on too long, its limited EXERCISE LEARNING Neurogenesis through meditation Some drugs help replenish hippocampus SSRIS promote neurogenesis in hippocampus (antidepressants) Hippocampus has cortisol receptors to remember stressful event well so you don't repeat it Problem if it doesn't stop feeding back, experience other problems!!! Adrenal gland cortex (outside) is stimulated inside to get adrenaline Super active amygdala says not safe gets stronger and hippocampus gets weaker, dysregulation start experiencing anxiety, further depression on a continuum Stress by itself not bad, chronic with don't control it is bad Event itself not your problem it's the way you perceive it It's your perception of the event! Social rejection affects anterior cingulate cortex Activate left hemisphere to make you happy, talk, move right side of body, role eyes to left Elevate DA and 5-HT Stress is in your control **EXAM: Neuroendocrine stress response, HPA (hypo, pituitary, adrenal) = crh , acth, cortisol feeds to hippocampus mostly and others Stress = an unpleasant and disruptive state resulting from the perception of danger or threat Stressor = is often used to identify a source of stress Chronic stress feeds repeatedly back to hippocampus, which will make it too toxic for cells and they start to die Stress can make you forget things, too much cortisol in general memory problems like exam forget Hippocampus has receptors to cortisol binding of cortisol (excitatory) becomes stimulant make you more aroused, right amount is the trick. Acute stress: initiates fight or flight and sympathetic nervous system, memories are vivid, most of energy is going to that response lion and serengeti, lion chase you would have very vivid memories, pay attention to more threatening stimuli Moderate amount of cortisol can enhance memory and the hippocampus but too much kills the cell.

Hippocampus Lambic System Cerebral cortex Describe cortex-morphology (i.e., lobes and critical gyri and sulci) and the associated functions of primary cortical areas and the cortical lobes.

Hippocampus: declarative memory formation, emotion, memory, autonomic nervous system Limbic system — collection of forebrain structures, participates in emotional behavior, motivated behavior & learning • ACC: cost benefit analysis, delayed gratification, Physical & emotional pain activation > amygdala: Fear, aggression, fear conditioning is processed Cerebral cortex — 4 lobes; Sensory cortex, motor cortex and association cortex, the outer layer of the cerebrum (the cerebral cortex ), composed of folded gray matter and playing an important role in consciousness. Central sulcus — Sulcus divides frontal and parietal lobe gyrus/cortex in front of division — primary motor cortex (precentral gyrus) Primary somatosensory cortex behind central sulcus Frontal Lobe: **executive functioning (decision making), personality, movement, language, most complex Broca's area (left frontal lobe): speech production Parietal Lobe — Primary Somatosensory cortex is located here on postcentral gyrus, touch, secondary cortex is also here for association Occipital Lobe — Vision Temporal Lobe — learning, memory, auditory cortex is located here Temporal lobe is divided from rest of brain by lateral fissure/sulcus Critical gyri (frontal lobe in front of central gyrus = primary motor cortex behind parietal lobe is primary somatosensory cortex) Pre/post central gyrus

Invasive v. Noninvasive

Invasive: histology (slices of brain), autopsy, lobotomy (prefrontal cortex damaged when separated from rest of brain i.e phineas gage), stimulation, lesion Noninvasive • Structure 1. CT: high resolution, exposed to x rays, X distinguish between living & dead brain 2. MRI: high resolution, image taken at any angle wo Movement from patient, stronger magnets affect behavior & safety • Function 1. PET: measures activity based on glucose & O2, exposed to radioactivity, low resolution 2. EEG: measures electrical impulses, diagnoses schizo, dementia, epilepsy, ADHD, some data lost 3. MEG:measures magnetic impulses (X lost), clearer pic, more freq, fast & quiet, localization of abnormal electrical activity • both 1. fMRi: track blood flow, more active = more blood flow

2. Describe the effect of the neurotransmitter on the postsynaptic membrane (e.g., IPSP's, EPSP's, and NT-receptor interaction.

IPSP make the current less negative EPSP make the current more positive • Sum of the EPSP and IPSP currents combine, converge at axon hillock, if some of that hits threshold then action potential occurs. • type of NT determines individual EPSPs and IPSPs. Alchol, inhibitory, GABA inhibitory Glutamate inhibitory all converge, won't hit threshold. • NT is a key, receptor is a lock. Depending on lock and key, opens a gate (ion channel) on post synaptic neuron receiving signal (dendrite and soma) • NT binds to a receptor, receptor is bound to certain ion channel, which opens because NT binds to that receptor. The effect of the neurotransmitter on the postsynaptic membrane • EPSPs are graded potentials that can initiate an AP in the axon, small depolarization is created • whereas IPSPs produce a graded potential that lessens the chance of an AP in an axon, small hyperpolarization is created. metabotropic/ionotropic: how NT interact with postsynaptic neuron

6. Compare and contrast the three classic theories of emotion.

James-Lange Theory ( Perceived stimulus → specific physical responses → subjective feeling) Physical response occurs first and inform subjective experience Awareness of our physical state leads to identification of a subjective feeling. Assumes physical states related to each type of feeling (sadness, happiness) are highly distinct from each other and we can correctly label these distinct physical states as separate feelings. Contrast Assumes we have specific physical states that map onto recognizable emotional states. This wasn't always the case because many emotional states are accompanied by overlapping physical sensation Cannon-Bard Perceived stimulus → physical responses, and subjective feeling (independent from eo) both the subjective and physical responses occurs simultaneously and independently physiological fight-or-flight response The CNS has the ability to produce an emotion directly without needing feedback from the peripheral nervous system. Schachter-Singer two-factor theory Perceived stimulus produces general arousal assessment of surroundings subjective feeling Two-factor theory is helpful in explaining how general arousal can intensify an emotion Theory assumes that emotions result from a sequence of events ■ Does not require specific set of physical responses for each emotion ○ Theory uses more of a top-down approach ■ Uses cognition appraisal of a situation ■ Memories and expectations to organize incoming sensory information Contrast ○ Assumption that physiological states are not uniquely associated w/ specific emotion

Korsakoff's syndrome Kluver Bucky syndrome Stress GAS Lobotomy

Korsakoff's syndrome — anterograde amnesia from thiamine (vitamine B1) deficiency, found in chronic alcoholics 2. James-Lang theory — person's physical state provides cues for identification of emotional state Kluver-Bucy syndrome — collection of symptoms, including tameness, extreme sexual behavior, & oral exploration; results from damage to temporal lobes (amygdala) Stress — unpleasant & disruptive state resulting from perception of danger/threat • Stressor — source of stress General Adaptation Syndrome (GAS) — 3 stage model for describing body's response to stress 1. Alarm response — activation of sympathetic NV & mental alertness > Fight/flight response 2. Resistance stage — efforts to maintain normal activities while coping w stress > Judgement & resistant to disease deteriorates 3. Exhaustion stage — extremely low reserves of strength & energy, causes depression Lobotomy —holes drilled in frontal lobe of brain, calms down institutionalized ppl

10. What is the evidence that learning and memory exists at the cellular level (hint: look at LTP)?

LTP = Long Term Potentiation (long lasting potentiated response on post synaptic side) -Amplysia invertebrate, simple forms of learning, sensitization and habituation, reduction and increase in NT substances in short term habituation and sensitization Long term, changes in structure in 5ht and ca+ influx increase, and increase connections receptors site Classical conditioning in aplysia in chapter LTP (learning): AP.... influx CA+ NT released and binds lock and key to receptor (if for glutamate excitatory... glutamate causes influx of positive current, PSP, more na+ goes in more depolarization you see the less, there's less Response lasts for a long time. It's a high burst of activity/current in rapid succession, open ion channels fast so AP's come during relative refractory period and come much faster , more CA+ more NT coming out, that paradigm in hippocampal slices in petri dish (elevated depolarization occurs) go away and come back, turn it back to regular stimulus, but see an increased/exaggerated response ANSWER* Pre and post synaptic changes in structure as a function of this (more receptors)!! Dendritic spines more collaterals presynaptically, more branches more spines post synaptically Function of temporal and spatial summation. *****Due to NMDA receptor NT have multiple receptors, key, lock, open door doesn't fully open but needs to be depolarized and have NT both voltage and chemical dependent. Glutamate NT bind to NMDA receptor, MG ion blocks part of channel so CA+ can't get in, but with both glutamate and depolarization at same time MG+ knocked out and channel opens so Ca+ can go in! Ca+ stimulates protein kinases enzymes that move proteins take AMPA receptor (bring glutamate receptor to surface)s and puts them up on surface, when glutamate comes out and binds to NMDA and binds to AMPA too. Produces a bigger effect. Another reason there's a bigger effect now more receptors and they stay there for a while. Post, and pre synaptics changes and they last a while, more receptors postsynaptic and more NT Learning and thinking this is all happening, changes the morphology of your synapses. More think, learn, exercise, sleep can change morphology in your hippocampus and the more AMPA and NMDA receptors post syn and glutamate presynaptic easier it is to learn. Perforant pathway, CA3, and goes down to Ca1 connections put stimulating electrode in their shot + current in, stimulates AP releases NT measure it in piece of hippocampus (PSP) excitatory, NT binds to AMPA or NMD receptor, but burst depolarization and NMDA receptor bound More receptors and NT coming out different response, learning and memory occurs as a result. LTP mostly ** in mammals mechanism for learning in hippocampus changes in pre and post synaptic connections trisynaptic loop between entorhinal cortex to CA1 -A type of synaptic plasticity in which the application of a rapid series of electrical shocks to an input pathway increases the postsynaptic potentials recorded in target neurons. -1970's researchers began to investigate the neural mechanisms in the hippocampus that appear to provide a basis for learning and memory -application of a rapid series of electrical shocks to one of these pathways increases the postsynaptic potentials recorded in their target hippocampal cells. Experience makes these synapses more efficient, The change in responsiveness in the target cells after the rapid series of shocks is LTP -Lasts indefinitely in a living animal, in an isolated blic slice lasts several hours. LTP = important memory device, improves consolidation of memories so we don't lose them strengthening of synapses is consolidation, multiple stimulus keeps stimulating cells forms pattern, can go back after a few hours stimulate once same effect (retrieval) Glutamate receptors, NMDA and AMPA receptors, when glutamate binds to AMPA receptors then the cell will become depolarized because glutamate is excitatory and depolarization knocks out MG+ that blocks the NMDA receptor, and now Glutamate can bind to NMDA receptor -----> meets the condition for both Glutamate binds to AMPA receptor, it means both pre and postsynaptic neurons are active (associativity) Cooperativity happens because both AMPA and NMDA receptors are activated, two different receptors activated two synapses are converges on the postsynaptic neuron. Cooperative and associate activity need to happen for LTP Associativity - both pre and postsynaptic neurons need to fire at the same time Cooperativity- which says 2 or more synapses need to converge on a postsynaptic neuron. Both of those need to happen for LTP Learning, keep stimulating circuit strengthening it Memory retrieval introduce small stimulus later and it still responds. Lasts a long time, some memories last for life Leads to structural changes in our brain, new pathways creating, It takes only seconds of input to produce LTP LTP occurs in ways predicted by the cellular learning model by Hebb

3. What is the limbic system and how is it involved in fear, aggression, and learning?

Limbic System — Is a collection of forebrain structures that participate in emotional behavior, motivated behavior and learning. • hippocampus (learning/memory, stress damages it) • amygdala (emotion, fear, rage, and aggression, and motivation, receives input from all the senses and sends the info to other limbic structures, fear conditioning) • hypothalamus (fighting, fornicating, fleeing, feeding, basic needs, hormone production) • cingulate cortex (empathy, social awareness, and self control) > Anterior Cingulate Cortex ACC is autonomic functions, decision making, error detection, emotion, anticipation of reward, empathy, emotional info about pain) ~ ACC lots to do with cost benefit analysis of what your doing, and the place with delaying gratification, and important in pain Physical and emotional pain activation > Posterior Cingulate Cortex PCC (eye movements, spatial orientations and memory, septal area, reward area) • olfactory bulbs (receive, process info about smell) • parahippocampal gyrus, mamillary bodies of diencephalon, and fornix (connects mammillary bodies and hippocampus) > These three involved in Memory processes • thalamus (relay system, sensory) • reward system of the nucleus accumbens (mesolimbocortical pathway) Aggression and fear amygdala, connects to hippocampus (learned/remembered) these two connect and get strengthened connections, amygdala becomes more active, creates stronger connection or circuit with hippocampus that pattern of learning becomes ingrained in the hippocampus, worried negative emotions also produces a lot of DA, brain might find that rewarding (reinforces the mesolimbocortical pathway and the nucleus accumbens)

Membrane Graded Potential IPSP & EPSP Concentration Gradient & Electrical Force Saltatory conduction Threshold AP Polarization, depolarization, hyperpolarization

Membrane — thin sheet of tissue/ ayer of cells acting as a boundary, semi-permeable due to lipid bilayer, selective as to what it allows to enter the cell; protects cell • Extracellular — Outside (NA+) & (CL-) • Intracellular — Inside (A-) & (K+) Graded potential — varies in size (not all or none), magnitude depends on stimulus strength • Special summation — input from many synapses added together to produce ap; combines input from different locations on dendrites • Temporal summation — single, very active synapse provides sufficient input to produce ap; accumulates over short time, proportional to stimulus IPSP's — small hyperpolarization (neg) produced in postsynaptic cell as a result of input from presynaptic cell EPSP's — small depolarization (less neg) produced in postsynaptic cell as a result of input from presynaptic cell Na+/K+ pump — uses energy, 3 Na+ out for 2 K+ ions in Concentration gradients — moving ions from high to low concentration Electrical force — opposite attract, same charge repel Saltatory conduction — movement of AP from node of ranvier to node of ranvier Threshold — level of depolarization => AP • Threshold depolarization — min level of depolarization to reach threshold/AP Polarization — neg Depolarization — less neg Hyperpolarization — change in membrane potential in more neg direction AP — nerve impulse arising in axon, all-or-none • Resting potential -70 mV • Na+ & Cl- outside • K+ & A- inside • inside more neg bc A- • propagation of AP — replication of AP down length of axon Absolute Refractory Period — production of 2nd AP unlikely/impossible regardless of input Relative Refractory Period — production of 2nd action potential possible in response to larger than normal stimuli

9. What brain regions are involved with anterograde amnesia?

Memory consolidation: encoding, consolidation (leaves hippocampus and goes somewhere else for long term storage), retrieval, reconsolidation HM removed temporal lobe tissue, hippocampus is essential for episodic and factual memories, declarative explicit, procedural was still able to be done nondeclarative. N.A. diencephalon fencing rod up through sinus, didn't hit hippocampus but went in dorsomedial thalamus and mammillary body (hypothalamus) diencephalon. ****** The primary structure involved in anterograde amnesia is the hippocampus, but damage to diencephalon structures, such as seen with NA and Korsakoff's syndrome, also produce anterograde amnesia. Korsakoff damages diencephalon part of it anterograde amnesia with confabulation (wild stories to cover deficits) The temporal lobe, hippocampus, both connected to thalamus Anterograde amnesia: memory loss for information processed following damage to the brain Temporal Lobe: -attain newly acquired procedural implicit memories while experiencing dramatic deficit in ability to form new explicit memories. Henry Molaison, patient H.M., child bike accident brain damage, seizures, got surgery, his hippocampus, amygdala, and part of the association cortex of temporal lobe removed both right and left hemispheres, seizures improved, and his personality vocab and above average IQ unchanged, remembered most of info acquired prior to surgery but anterograde amnesia profound, issues transferring new info on people, places, events, numbers from STM to LTM Procedural memory was fine, STM fine Medial temporal lobe affects declarative but not nondeclarative memory Old LTM fine, but storing STM to LTM bad Patient N.A. - the diencephalon and memory, hippocampus and other areas of the temporal lobe are connected with thalamus. Disruption leads to amnesia, dicephalic lesions, brain damage freak accident stabbed through nostril with a mini fencing foil, lesion in his left dorsomedial thalamus, mammillary bodies, and mammillothalamic tract, anterograde amnesia and some retrograde amnesia, STM and intelligence preserved, absence of hippocampal damage still had difficulty forming new declarative explicit memories. Squire, Tower of Hanoi puzzle anterograde amnesia patients, could solve it but not remember it nondeclarative procedural memories were fine. Chronic alcoholics amnestic confabulatory neurocognitive disorder (Korsakoff's) anterograde amnesia, deficiency of thiamine B1 vitamin helps make ACh, untreated thiamine deficiency leads to damage in the dorsomedial thalamus and mammillary bodies of the diencephalon

12. What causes depression and what is the treatment? Is this different from bipolar disorder?

NE and Serotonin, diet, exercise lack, stress can cause it, prenatal environment, genetics, reduction in serotonin (low monoamines in general). Schizo is high DA. One theory says depression can be caused by low serotonin levels Bipolar some, NE manic stage, medicine. Root causes are different, lithium in bipolar works but doesn't work for depression. Interplay of factors cause it. Bipolar disorder: A disorder associated with episodes of mood swings ranging from depressive lows to manic highs. Bipolar/MDD, MDD more in women, bipolar, equal men and women. Two categories of mood disorder: (COPY picture) Major depressive Causes: problems in HPA axis, showed growth hormone, thyroid hormone levels, cortisol levels high, continuum of stress (depression and anxiety), amygdala turn on hypothalamus to release Synthetic cortisol, dexamethasone test (DST) to healthy person see less cortisol from person, given to depressed person, they can't turn it off. Stress response. Indicated major depression and chronic stress. 5 HT more serotonin, feel better from SSRI, combo of things causes it. SSRI do what exercise do, CBT, medication, exercise, ECT, meds plus psychotherapy ALSO increase neurotrophins. Keeps cells from killing themselves (apoptosis), preserves them, increase neurogenesis. In hippocampus! SSRI elevate 5ht, but also do this that takes five weeks. Brain derived neurotrophic factor. Deprive yourself of sleep (<6 hours; 1-2 nights) is the best!!! MAO inhibitors suppress MAO which breaks down monoamines Genetic contribution, genes play moderate role in MDD, heritability of depression in twins appears to be 40% Number of genes involves including those involved with serotonin reuptake and the genes that regulate circadian rhythms Specific single nucleotide polymorphisms correlated with MDD Variations of serotonin transporter gene one or two copies of the short form (vs long form) much more likely to develop depression if stressed Environment also Prenatal events, stress, larger and prolonged release of cortisol particillay in people with the short versions of the serotonin transporter gene Brain structure and function, see a reduce volume of hippocampus and orbitofrontal cortex, abnormal ACC activation, happy mood more activity in left cerebral hemisphere, depression has reduced activity in left frontal lobe and increased activity in the right frontal lobe Abnormalities in monoamine activity, and serotonin less if depressed Abnormalities in glucocorticoid release in HPA axis due to stress Lower levels of major byproduct of dopamine Abnormal density and sensitivity to receptors in NE in prefrontal cortex less NE Treatment for depression: Most common is prescription of antidepressant meds, SSrI usually Therapy Exercise ECT electroconvulsive therapy, if don't respond to meds or CBT Deep brains stimulation stimulation electrode implanted surgically in white matter of cingulate cortex both hemispheres constant stimulation CBT

Nucleus Autoreceptor Enzymatic deactivation & reuptake Neuromodulator

Nucleus — contains cell's DNA Autoreceptor receptor — on presynaptic neuron, provides info about cell's own activity levels • Ionotropic receptor — postsynaptic membrane, recognition site on same structure as ion channel • Metabotropic receptor — postsynaptic membrane, recognition site & G protein > NCs binding to these receptors X directly open ion channels, slow but long term changes Enzymatic deactivation — enzyme consumes NTs to stop its effects Reuptake — ends action of NCs in synaptic gap, presynaptic membrane recaptures mols of NTs • ACh deactivated w AChE (enzyme), everything else => reuptake Neuromodulator — chemical messenger that comm w target cells more distant than synapse by diffusing away from point of release.

Parkinson's disease Medial forebrain self stimulation Gate theory of pain Dorsal & ventral streams

Parkinson's disease — degenerative disease, difficulty in moving, muscular tremors, frozen facial expressions • damage of basal ganglia (voluntary movement control) Medial forebrain self-stimulation — electrical stimulation of the medial forebrain bundle (feel pleasure & rewards) Gate Theory of Pain — explanation of effects of context on pain perception • Theory explains variability of pain: Sometimes let pain signal go up to brain sometimes close the gate and we don't. • How do we close the gate so pain signal doesn't get up? > Morphine closes gate, binds to endorphin receptors in periaqueductal grey region in midbrain, efferent descending signals go down & inhibit pain signals from going forward >Hypnosis can stimulate PAG/distractions to inhibit pain or stress closes descending gate The Secondary Extrastriatal pathways (i.e. dorsal and ventral streams): • Dorsal Stream — pathway leading from primary visual cortex in dorsal direction > MST (medial superior temporal lobe) → parietal lobe > For perception of movement. • Ventral Stream — pathway of info from primary visual cortex → inferior temporal lobe → temporal lobe & fusiform >Processes object recognition.

Planes of Dissection Sections

Planes of dissection • Rostral — toward the head of a animal/front of head • Caudal — towards the tail/back of head • Ventral — front belly area • Dorsal — back • Neuroaxis — imaginary line that runs the length of the spinal cord to the front of the brain • Anterior — front • Posterior — back • Superior — above • Inferior — below • Midline — imaginary line divides body in two halves • Ipsilateral — same side of midline • Contralateral — opposite sides of midline • Medial — toward midline • Lateral — away from midline • Proximal — closer to center, for limbs • Distal — farther away from another structure SECTIONS • coronal/frontal section — divides brain front to back parallel to face • Sagittal section: — parallel to midline > Midsagittal sagittal section — divides the brain into two equal halves • horizontal/axial/transverse — divides brain from top to bottom.

11. What are short- and long-term memory? Where is explicit memory consolidated, and what does the hippocampus have to do with it?

Short Term Memory: An intermediate memory store in which limited amounts of data can be held for a limited amount of time, without further processing. Such information is permanently lost. Small, 5-9 items, AND lasts up to 15-18 seconds Long Term Memory: A memory store in which apparently unlimited amounts of data can be held for an unlimited amount of time, unlimited capacity and duration Explicit (Declarative memory) is consolidated in the hippocampus, and the hippocampus has to do with it because... Essentially brain two copies of memory, rehearse memory and it gets reconsolidated Memory in hippocampus another copy is made goes to various parts of (cerebral cortex )various parts of our brains) Memory doesn't stay in hippocampus, more like stays there and reorganizes memory and goes to various parts of brain and its cemented in cerebral cortex and various parts of brain.

1. Describe the stimulation and conduction of an action potential.

Stimulation comes from a presynaptic neuron releasing NTs. NTs are collected by the receptors on postsynaptic neuron, open ligand-gated ion channels. Cause enough depolarization at axon hillock to open Na+ channels and Na+ flows out, Na+ channels close, K+ channels open, become inactive, hyperpolarize. Process of action potential (Extracellular) Outside cell membrane: (NA+) & (CL-) (Intracellular) Inside cell membrane : Anion (A-), & K+ Semi-permeable membrane of axons Action potential steps: Resting membrane potential = -70 millivolts (mV) 1) Stimulus arrives 2) Stimulus needs to push above -70 mV, meets threshold 3) Triggers AP 4) Na+ channels open & it heads inside caused by concentration gradient, attracted inside bc inside is negative compared to outside which is positive. Also more Na+ outside > inside 5) depolarization inside cell. Peak inside cell +40 mV (when it hits the peak absolute refractory period Na+ channels become inactive) . So much K+ leaves Relative refractory need more negative to hit threshold so much K+ leaves cell it's way below negative -70 way more negative. 6) Channel opens later than sodium is K+ which goes outside, (factors which make it go outside are concentration gradient, cell more positive compared to outside, also a little bit of electric charge going out) 7) Past -70mV Na+ leaves = whole process = action potential 8) Na+ channels become inactive close at +40 mV no more Na+ enters cells, K+ keeps leaving and cell becomes negative again, and goes back down again +40 action potential at peak K+ leaves and NA+ stops coming in, mid-way of action potential **Artificial part of the process, not worried about the neuron and stimulus being delivered, if we stick an electrical stimulus and stimulate axon hillock with a certain voltage and push above the threshold it causes an action potential Influx of Ca+ at axon terminal releases NT

SCN REM rebound Narcolepsy Sleep paralysis Insomnia Zeitgeber

Suprachiasmatic nucleus (SCN) — area of hypothalamus above optic chiasm, maintains circadian rhythm REM rebound — ↑ amt REM sleep following period of REM deprivation, antidepressants suppress & delay REM • Narcolepsy — intrusion of REM sleep & REM paralysis into waking state. > Enters REM immediately & awaken feeling refreshed > Cataplexy — REM muscle paralysis intrudes into waking state > Sleep Paralysis — REM muscle paralysis occurs preceding/following actual sleep • Insomnia — difficulty initiating or maintaining enough sleep to feel rested > Onset Insomnia — difficulty getting to sleep at bedtime > Factors: stress, anxiety, stimulant drugs > Maintenance insomnia — can't stay asleep during the night > Factors: stress, substance use, psychopathology > Treatment: regulating sleep schedule, avoid stimulants, medications (benzodiazepines, other sedatives) Zeitgeber — external cue for setting biological rhythms, light = most important zeitgeber • Internal biological clocks interact with zeitgeber stimuli • Free-running circadian rhythm — rhythm X synchronized to env time cues > Occurs in a sense of natural light: Exposure to sunlight helps reset/entertain internal biological clock ~ Entertainment — resetting of internal biological clocks to 24-hour cycle of earth's rotation

5. What is the role of the SCN in circadian rhythms? (body's internal master clock)

The SCN (Suprachiasmatic Nucleus) is an area of the hypothalamus located above the optic chiasm; responsible for maintaining circadian rhythms. It is the body's internal master clock. *Circadian rhythm: A repeating cycle of about 24 hours. • SCN helps to distinguish day and night. Produces a response to sympathetic nervous system, which in turn communicates with the Pineal Gland, as light decreases in evening, pineal gland synthesizes and releases more Melatonin, a neurochemical modulating brainstem structures related to waking and sleep. Manages also other sleep related changes, such as body temperature, hormone secretion, production of urine, and blood pressure changes. The SCN is not dependent on input from other structures to maintain its rhythms. Acts as master clock that coordinates activities of other internal peripheral clocks that exist in most body cells. The rhythms of SCN are influenced by info about light made by retinohypothalamic pathway, peripheral clocks influenced by daily feeding cycles. The SCN is only active during the day On a cellular basic, oscillation of protein production and degradation within a cell, ebb and flow of special circadien proteins. Three separate genes and their protein products involves with cellular circadian rhythms, per, tim, and clock. • Per and tim together inhibit clock, and clock promotes production of per and tim • As levels of per and tim increase inhibition of clock ensures no more per and tim produced when per and tim protein level drops over time the reduced inhibition of clock results in increased production of per and tim