Neurobiology 572 Final

Where do preganglionic axons from the parasympathetic NS emerge from?

Emerge only from the brain stem & Sacral region

What is Leptin? What produces it & what role does it play?

Leptin = a hormone produced by fat cells that acts directly on the arcuate nucleus (in the hypothalamus) Leptin regulates body mass & E-intake

What is the function of the Locus Coeruleus? What areas do its neurons project to?

Locus Coeruleus projects to several areas of the CNS = e.g. spinal cord, cerebellum, thalamus, cerebral cortex *It innervates everywhere EXCEPT the striatum! (can rlly influence any part of brain) Function: -source of brain [NE] Regulates: - Attention* - Arousal* - Sleep-wake cycle - Learning* - Memory - Anxiety* - Pain - Mood* - Brain metabolism The Locus Coeruleus influences Attention, Anxiety, Arousal, Learning & Mood

How does the Nucleus of the Solitary Tract influence feeding?

The nucleus of the solitary tract is located in the medulla (brain stem) & is an important center for autonomic control Gastric distention & cholecystokinin = send satiety signals to the nucleus via the vagus nerve, activating the nucleus & inhibiting feeding behavior

Where is the nucleus of the solitary tract located? How does the contribute to it's function?

The nucleus of the solitary tract is located in the medulla (brainstem) -this allows it to act as another center for autonomic control bc many ANS preganglionic neurons originate in the brainstem, so the nucleus of the solitary tract is able to influence the output of the ANS brainstem nuclei.

What are some examples of sympathomimetic drugs?

1) Atropine = antagonist of mAChRs -producing signs of the sympathetic N.S bc it inhibits paraysmp 2) Amphetamine = appetite suppressant & parasymp antagonist 3) Salbutamol = B2-adrenergic receptor agonist -treats asthma via bronchodialtion = symp activator

What are the two neural circuits for anger & aggression?

1) The Predatory Aggression/ Silent-Attack Pathway: -Lateral Hypothalamus / Medial Forebrain Bundle (this has been involved motivated behavior) -Medial Forebrain Bundle projects to the VTA 2) The Affective Aggression/ Threat-Response Pathway: -Medial Hypothalamus neurons project to the Periaqueductal gray matter (PAG) of the midbrain

What is the route of the ANS fibers?

1. ANS preganglionic fibers emerge from the spinal cord & the CNS (specific brain nuclei) 2. ANS pregnaglionic fibers then synapse within autonomic ganglia onto the postganglionic fibers 3. Postganglionic fibers then travel to smooth muscles, cardiac muscles, glands --> ANS influences targets in a disynaptic pathway (uses interneurons ?)

What are the two theories on emotions?

1. Basic Emotions Theory: -specific emotions =indivisible & innate / universal Fear, Anger, Disgust, Happy, Surprise, Sad -each emotion = specific neural & phys response -correlates to Darwins ideas 2. Dimensional Theories of Emotions: -emotions can be broken down into smaller fundamental elements -emotions consist of differing amounts of brain activation corresponding to different affective* dimensions /subpatterns (e.g. pleasantness, emotional strength)

What are the two states of eating & what kind of metabolism are they associated with?

1. Prandial State - just ate; performing anabolism / anabolic metabolism -means "upwards" 2. Postabsorptive Sate - fasting state; catabolic metabolism is occurring -means "downward" -think catapult = destroys things

What is the balance of E that needs to be achieved by eating?

E reserves are replenished @ the same rate that they expended / used. Intake > Expenditure = obesity Intake < Expenditure = starvation

Which division of the ANS has longer preganglionic neurons?

The parasympathetic preganglionic neurons are longer, they have to travel farther

You've stayed up all night trying to meet a term paper deadline. You are typing frantically, keeping one eye on the paper and the other on the clock. How does the periventricular zone of the hypothalamus orchestra physiological response to stressful situation?

The periventricular zone of the hypothalamus has direct innervation control of the posterior pituitary and the anterior pituitary. The AP acts as a gland and produces hormones that has many downstream effects. The AP is controlled by the periventricular zone of the hypothalamus via the parvocellular neurosecretory cells that release hypophysiotropic hormones that travel via the hypothalamo-pituitary portal circulation to the AP 1. The response begins by the parvocellular neurosecretory cells determining this paper deadline to be a stressful stimulus & then releasing corticotropin-releasing hormone (CRH) 2. CRH travels to the AP via the hypothalamo-pituiary portal circulation, and causing the release or corticotropin from the AP --> corticotropin = adrenocorticotropic hormone (ACTH) 3. Corticotropin / ACTH released from the AP travels through bloodstream and reaches the adrenal cortex 4. The Adrenal Cortex releases cortisol, which is a steroid hormone that induces the physiological response of stress --> mobilizes E reserves, and suppresses immune response

What is the purpose of the pituitary gland in maintaining homeostasis?

The pituitary gland is how the hypothalamus is able to control the body's homeostasis functions. The hypothalamus tells the pituitary when and what hormones to product and spread through the body!

NPY and AgRP are considered.....

orexigenic peptides -they are appetite-stimulating

What produces insulin?

the B-cell of the Pancreas

What NT agonists and antagonists would you design to treat obesity? Consider drugs that act of brain neurons, as well as peripheral N.S.

-Antagonist of MSH -Antagonist of AgRP -Antagonist of NYP -Antagonist of Orexin -Antagonist of Ghelin -Agonist of aMSH -Agonist of CART -Agonist of Leptin -Agonist of Cholecystokinin (CCK) -Agonist of satiety signals / gastric distention --> agonist of sensory mechanoreceptors of stomach wall

Depression is associated with...

-Hyperactivity of HPA axis (lowered GCRs in hippocampus...) -Hyperactivity of anterior cingulate cortex Effective Ads target & reduce this

What is the Enteric NS? Where is it located? What are the divisions of the enteric NS? What dose the Enteric NS control?

-It is a division of the ANS -referred to as the "little brain" -500 millions neurons Located in the lining of the esophagus, stomach, intestines, pancreas, & gallbladder (in the gastrointestinal tract!) Divisons: 1. Myenteric (Auerbach's) Plexus 2. Submucous (Meissner's) Plexus Plexus = a network of nerves / vessels Function: it controls the physiological processes of transport & digestion of food from oral --> anal openings

What are the two key players that regulate / limit food intake?

-Leptin -Arcuate Nucleus in the Hypothalamus

Are there any sex differences in fear expression?

-Males tend to freeze -Females tend to flee/dart

Which NTs are catecholamines?

-NE -DA (hormones made by the adrenal glands)

What are Amine NTs ?

-Norepinephrine (NE) -Dopamine (DA) -Serotonin (5-HT) -Acetylcholine (ACh) -histamine -epinephrine (pretty much all the ones we talk about are amine NTs)

What are the subdivision of anxiety disorders?

-Panic Disorders -Agoraphobia -PTSD -OCD

What are the NT's used by the sensory and motor components of the enteric NS?

-Serotonin (5-HT) -Dopamine (DA) -Acetylcholine (ACh)

Which NTs are monoamines?

-Serotonin (5-HT) -NE -DA

What are the diffuse modulatory systems and what are their general functions / features ?

-These are small centers within the brain responsible for overall [ ] of their specific NT General Function: -They perform regulatory functions, modulate postsynaptic neurons General Features: 1) They are groups of specific cells that produce a specific NT, each core = a small set of neurons, which is really several thousand 2) They arise from the central core of the brain, most from brain stem 3) Extensive projections / axonal branching - each neuron could have 100,00 postsynaptic connections 4) They release NT into extracellular fluid (extra-synaptically) so that it can effect higher # of synapses

What are some ways feeding behavior is regulated in a short-term sense?

-how long since we last & how much we ate that time -when eating, it determines motivation to keep eating based on how much & what type of food has been consumed

What are the three phases of feeding behavior?

1. Cephalic Phase: -site & smell of food trigger activation of parasymp N.S & Enteric ANS = secrete saliva in mouth & digestive juices in the stomach 2. Gastric Phase: -gastric activity begins w/food in stomach (gastric distention) 3. Substrate Phase: -stomach fills w/food = partially digested food moves to intestines to absorb nutrients (Cephalic = head...think of the sensory systems on head = site & smell)

What are the two common CNS stimulants that we learned about?

1. Cocaine 2. Amphetamine --> CNS stimulants act by influencing the dopaminergic (DA) and noradrenergic (NE) system's synapses. -DA & NE = catecholamines; both excitatory NTs They stimulate enhanced catecholamine release = sympathomimetic...cause peripheral effects like increased heart rate & BP, dilated pupils

Serotonin in different functions:

1. Eating Disorders: -abnormal / low serotonin levels have been associated with E.Ds, can be helped with drugs that increase the [5-HT] 2. Aggression Serotonin Deficiency Hypothesis = low serotonin levels facilities aggression, specifically the 5-HT1 receptor 3. OCD: -families with rare mutation in 5-HT transporter gene that made it extremely efficient = high incidence of OCD. -SSRIs can be used to treat OCD 4. Monoamine Hypothesis for Affective Disorders: Depression is the consequence of a depletion in 5-HT and NE (Reserpine = depletes monoamines/ bad & Desiparamine = acts as 5-HT and NE SRI = antidepressant)

What are two satiety signals that occur while we are eating? By what mechanism are they transduced?

1. Gastric Distention -stomach stretching sensed by mechanosensory axons in stomach wall 2. Cholecystokinin (CKK) -satiety peptide released by intestinal cells in response to stimulation of intestines by specific foods (esp fatty ones) Both gastric distention & Cholecystokinin signals are sent to the Nucleus of the Solitary Tract by the Vagus Nerve! -activation of NST = inhibition of feeding -CCK and gastric distention work synergistically to inhibit feeding

What are some diseases that were found to be of biological basis?

1. General Paresis of the Insane -among institutionalized ppl -mania --> cognitive degradation --> paralysis --> death -found that it was actually caused by bacterial infection (T Pallidum) + could be treated w/penicillin 2. Vitamin Deficiencies 3. HIV into brain = dementia

What are the two forms that E is stored in?

1. Glycogen -kept in liver & skeletal muscle 2. Triglycerides -kept in adipose tissues

What are the three responses of the Hypothalamus from a break in homeostasis? What part of the hypothalamus performs it?

1. Humoral Response: stimulates or inhibits release of pituitary hormones into bloodstream 2. Visceromotor Response: adjust ANS outputs 3. Somatic Motor Response: incite appropriate behavior response -Humoral & Visceromotor Responses = controlled by the Periventricular zone; these responses automatically kick in -Somatic Motor Resp is controlled by the Lateral zone of Hypothalamus

What is the hormone released by each aspect of the HPA axis?

1. Hypothalamus' parvocellular neurosecretory cells produce Corticotropin-releasing hormone (CRH) 2. Anterior Pituitary releases Corticotropin / Adrenocorticotropic hormone (ACTH) 3. Adrenal Cortex produces Cortisol CRH --> ACTH --> Cortisol

What are the three functional zones of the Hypothalamus? And what are the general functions of each?

1. Lateral 2. Medial 3. Periventricular Functions: -The lateral & medial are highly connected to the brain stem & the telencephalon; and they relate to behavior! -The periventricular zone has 3 functions: 1. the Suprachiasmatic nucleus (SCN) gets retinal innervation & synchronizes circadian rhythms w/the light and dark cycle 2. controls ANS innervation output 3. Neurosecretory neurons = connect to & influence the pituitary's function

What occurs when Leptin levels are too low?

1. Low leptin levels activates arcuate nucleus neurons to produce: -Neuropeptide Y (NPY) -AgRP Humoral: -NPY & AgRP inhibit the paraventricular nucleus = lowered TSH and ACTH production, to lower metabolic rate & conserve E Visceromotor: -NPY & AgRP activates parasympathetic N.S Somatic Motor : -increases feeding behavior

What NT's do the neurons of the lateral hypothalamus contain?

1. MCH = melanin-concentrating hormone (peptide hormone) -MCH = strong orexigenic -when leptin is low, MCH is high MCH-lateral zone nuerons innervate most of cerebral cortex, where the organizing & initiating of goal-directed behaviors occurs (may contribute to motivation to seek out food) 2. Orexin = orexigenic peptide -lower leptin = high Orexin -imp in wakefulness

Treatment for schizophrenia?

1. Neuroleptics = target D2 receptors (also targets DA in the SN, causing Tarditive Diskinea, and symptoms of Parkinsons) 2. Atypical neuroleptics (e.g. clozapine) - don't act directly on D2 Hopeful to create drug that increases NMDA responsiveness

What are two possible theories on Schizophrenia ?

1. Over activation of Dopamine neurons -Amphetamine OD = positive symptoms 2. Under activation of NMDA receptors (Glutamate) -Ketamine & PCP OD = + and - symptoms -both of these drugs = inhibit NMDA receptors -possibility of cortical Glutanergic neurons in cerebral cortex...bc PCP only binds when NMDA is already open, need area thats ongoing / continuous activation

Via control of the Hypothalamus (periventricular zone), what hormones are released by the posterior pituitary, and what are their functions?

1. Oxytocin -"love hormone", it is released during sex / intimate behavior -promotes social bonding -promotes child birth by causing the uterus to contract - *lactation* 2. Vasopressin / antidiuretic hormone (ADH) -regulates blood volume and salt concentration -Vasopressin acts directly on the kidneys, creating water retention & reduced urine production -maintains blood pressure / volume via kidney communication (antidiuretic literally means to stop urine production, aka maintaining blood pressure, volume, fluid balance)

How does the HPA axis function? What is the flow of the pathway?

1. Parvocellular neurosecretory cells of the hypothalamus determine if that a stimulus is stressful and releases Corticotropin-releasing hormone (CRH) 2. Via the hypothalamo-pituitary portal circulation, CRH reaches the anterior pituitary and stimulates the AP to release corticotropin (adrenocorticotropic hormone / ACTH) 3. ACTH travels via the bloodstream & reaches the adrenal cortex, which then produces cortisol 4. Cortisol (a steroid hormone) can pass through the blood-brain barrier & inhibit CRH release by the parvocellular neurosecretory cells of the hypothalamus = negative feed-back

What are the two forms of aggression?

1. Predatory Aggression: -attacks against a member of the opposite species to obtain food -goal-directed behavior -involves few vocalizations -lunges @ neck -no sympathetic response 2. Affective Aggression: -killing for show, not for food -uses vocalization and threatening / defensive behavior or posture -self-defense -high levels of sympathetic activation

What are three components of the N.S that can act over great distances and an extended period time?

1. Secretory Hypothalamus -secretes chemicals directly into the bloodstream 2. Autonomic Nervous System -controls responses of internal organs, blood vessels, glands 3. Diffuse Modulatory Systems -cell groups with extended axonal projections & use metabotropic postsynaptic receptors -regulate arousal and mood

What are the diffuse modulatory systems for Dopamine (DA)?

1. Substantia Nigra (SN) 2. Ventral Tegmental Area (VTA)

What pathways occur once you are done eating a meal?

1. The Nucleus of the Solitary Tract alerts the brain that your are getting full & activates the parasympathetic ANS 2. Descending Vagus Nerve dilates blood vessels in intestines to absorb nutrients & stimulates release of digestive enzymes & insulin NST --> P.ANS --> B-cells --> Insulin

What are the two brain structures that directly create aggressive behavior?

1. Ventral Tegmental Area: -stimulated by the Lateral Hypothalamus (including Medial Forebrain Bundle) -Predatory Aggression 2. Periaqueductal Gray Matter of the Midbrain: -stimulated by the Medial Hypothalamus -Affective Aggression

What are treatments for affective disorder?

1.Electroconvulsive Therapy 2.Antidepressants: -Tricyclic Compounds = block NE + 5-HT reuptake, block ACh (Impiaramine) -SSRIs (Prozac) -NE & 5-HT SRI's (Effexor) -MAO inhibitors (block 5-HT and NE degradation) 3. Deep Brain Stimulation

What experiment was done to understand reinforcement and reward circuits?

1950s = Milner Rat Experiments: Had lever that rats pushed = ICSS / Intra-cranial self-stimulation (Electrical Self-Stimulation) ICSS = provided a reward that reinforced the behavior to press the lever -often chose lever over food/water Areas of self-stimulation was the Mesocorticolimbic DA Pathway (Mesolimbic DA Pathway) DA = enhances/reinforces learning DA = influences motivated behavior If you block DA, the ICSS decreased

What is the NT receptor that is believed to be directly involved in aggression?

5-HT1 Serotonin Deficiency Hypothesis: -Blocking serotonin synthesis / release = increases aggressive behavior 5-HT1 agonists = low aggression 5-HT1 antagonists/blocks = increases aggression

Each diffuse modulatory system core has ~ how many neurons?

A small set of neurons = ~several thousand

What is the function of the ANS & what is it control by? What are its divisions? What effects does it have?

ANS = under visceral control! Controls organs, blood vessels, glands. The ANS is controlled by the periventricular zone of the hypothalamus. The periventricular zone regulates the output of ANS innervation. Subdivisions: -Sympathetic N.S -Parasympathetic N.S Its functions are multiple, widespread, and relatively slow. -the activity levels of the two ANS systems are reciprocal

What is the outcome of abnormalities in serotonin regulation in terms of feeding behavior?

Abnormalities in brain serotonin contributes to eating disorders: -E.Ds = commonly accompanied by depression = lowers 5-HT levels & disturb eating habits E.Ds can be improved by drugs that increase brain 5-HT levels

An "Addison Crisis" describes a constellation of symptoms that include extreme weakness, mental confusion, drowsiness, low BP, and abdominal pain. What causes these symptoms and what can be done to treat them?

Addison Crisis is also known as Adrenal Insufficiency or Hypocortisalism --> Adrenal Insufficiency is caused by a disorder of the adrenal cortex which causes insufficient production of cortisol Addison's Crisis can be caused by the therapeutic use of corticosteroids = Prednisone, a synthetic version of cortisol .... when taking it, it fools the brain into thinking that cortisol levels are too high, so then it halts natural cortisol production...if one abruptly stops taking Prednisone, then there won't be enough time to rebound natural levels causing the adrenal insufficiency --> in addition to those who abruptly stop hormone replacement therapy, it is also common in those whose bodies don't respond to hormone replacement therapy in general. --> Cushings Disease, caused by a pituitary dysfunction, leads to elevated levels of ACTH levels bc the AP is not functioning to control the ACTH release...causes symptoms of an Addison's Crisis --> Can be treated by oral corticosteroids --> Prednisone

What Is Addison's Disease? What is Cushing's Disease ? What is the commonality between the two disorders? How are they different?

Addison's Disease: occurs when body does not produce enough Cortisol -adrenal insufficiency -causes fatigue, low BP, weight loss, etc. Cushings Disease: occurs when there is a dysfunction of the pituitary and it causes elevated ACTH levels -causes weight gain, immune suppression, sleepiness, memory impairment, irritable Common: both are dysfunctions of the same pathway, the HPA axis / the stress response Different: -they vary in the way Addison's Disease shows what happens when HPA axis / cortisol is down-regulated too much (no blood glucose release = weight loss & fatigue, low BP) -on the other hand, Cushing's Disease show's an up-regulation of the pathway by too much glucose release = weight gain, too much immune suppression, etc.

what neurohormone is produced by the Adrenal Medulla?

Adrenaline / Epinephrine

What is Adrenaline & what is released by?

Adrenaline is epinephrine. It is made from norepi & has almost exact effects of it -It has identical effets to that of the sympathetic N.S Produced by the adrenal medulla

What is the other name for Corticotropin?

Adrenocorticotropic-releasing hormone / ACTH

What is the state in which you have just had a meal, and what is occurring?

After meal state when the blood is filled w/ nutrients = Prandial State E is stored in glycogen & triglycerides Glycogen = finite capacity, stored in the liver & skeletal muscles Triglycerides = unlimited capacity, stored in adipose tissues In this state, anabolism / anabolic metabolism is occurring! (assembly of macromolecules glycogen & triglyceride from simple precursors to store E) (Prandial means dinner / lunch)

What is the relationship bw AgRP and aMSH?

AgRP and aMSH are antagonistic NT's They both bind to MC4 receptor in the lateral hypothalamus: -aMSH binds & inhibits = reduces feeding (anorectic) -AgRP binds & stimulates feeding (orexigenic) MC4 activation = normally stimulates feeding

Where did we originally see amphetamine used as?

Amphetamine was originally given to soldiers to keep them alert in combat, used as diet pills, or "pep pills" -Amphetamine is a CNS stimulant that blocks the reuptake of NE & DA, while also stimulating DA release

Based on fMRI / PET activity, what brain region is most activated by fear? sadness?

Amygdala = Fear Medial Prefrontal region = Sadness

What is the primary function and features of the amygdala?

Amygdala = in the temporal lobe, next to hippocampus. It is highly conserved circuitry among many species: -reciprocal interactions w/PFC It is a complex of nuclei: 1. Basolateral Nuclei -receives visual, auditory, gustatory, and tactile afferents 2. Corticomedial Nuclei: -receives olfactory afferents 3. Central Nucleus The Amygdala receives afferents from neocortex of all the lobes, the hippocampus & cingulate gyri Interconnections allow for the integration of info from all the diff sensory systems! Function: -fear & aggression *Recognition of fear* *Ability to fear*

What roles does Insulin play in Anabolism? Catabolism?

Anabolism: Insulin allows glucose to be transported into its storage locations = liver, skeletal muscle, fat *E storage = critical to survival Catabolism: Insulin allows for glucose to leave its storage sites & travel to various cells / body regions for fuel-use! *Needed for cell metabolism!

What is the most common psych disorder?

Anxiety Disorders: the inappropriate expression of fear -affects 15% of the pop -2x more common in females

Commonality of disorders:

Anxiety disorders = most common psych disorder (2x more in women) MDD = most common mood disorder MDD + DD = 2x more in women

What are the treatments for anxiety disorders?

Anxiolytic Drugs: 1. Benzodiazepines: make the GABAa receptor more responsive to GABA (ethanol = acts as an anxiolytic by binding to GABAa, thus why alcoholism & anxiety together = common) -GABA = fast, inhibitory Ex) Valium 2. SSRI's = block reuptake of serotonin, chronic use = increased glucocorticoid receptors = enhanced stress response regulation Ex) Prozac 3. B-Blockers = able to prevent onset of physiological symptoms by blocking NE signaling (blocking the sympathetic response of stress) Ex) Propanol

Compare & contrast the functions of the three regions of hypothal = arcuate nucleus, subfornical organ, and the vascular organ of the lamina terminalis.

Arcuate Nucleus - involved in feeding stimulation / inhibition. Has both aMSH and CART arcuate nucleus neurons that inhibit eating; while also having AgRP and NPY arcuate nucleus neurons that increase appetite / eating. Subfornical organ - involved in Vasopressin release in times of lowered blood volumes or pressure...this is involved in pathways that trigger thirst: Hypovolemia / low blood volume & Hypertonicity / increased solute levels Vascular Organ of the Lamina Terminalis = OVLT - involved in the thirst pathway triggered by hypertonicity. The OVLT neurons directly excite the magnocellular neurosecretory cells that produce vasopressin and creates the strong motivation to seek out and drink water.

What is the Ascending Reticular Activating System? What brain regions are involved?

Ascending Reticular Activating System = the Locus Coeruleus (NE) + the Raphe Nuclei (5-HT) are important in regulating wakefulness and sleep-wake cycle

What is another name for the Myenteric Plexus? (enteric NS)

Auchbach's Plexus

What is the function of the Basal Forebrain Complex in terms of it's specific NT?

Basal Forebrain Complex = ACh-neurons -Projects to the cerebral cortex, hippocampus, neocortex (Medial Septal Nuclei innervates hippocampus) (Basal Nucleus of Meynert innervates neocortex) Overall function = relatively unknown! -This area (esp Basal Nucleus of Meynert) dies in Alzheimers Disease -implicated in regulating arousal and sleep-wake cycle -implicated in memory formation & learning

What are the targets of anti-anxiety drugs?

Benzodiazepines target & enhanced GABAa activity SSRIs enhance serotonin B-Blockers reduce ANS effects

The blood vessels of the skin & sweat glands are only innervated by what division of the ANS? The lacrimal glands are innervated by what division of the ANS?

Blood vessels of the skin & sweat glands are only innervated by the symp NS Lacrimal glands are only innervated by the parasymp NS

New possible depression drug?

CRH antagonist

What category does Corticotropin-releasing hormone (CRH) fall under?

CRH is produced by the parvocellular neurosecretory cells of the hypothalamus They are also hypophysiotropic hormones

In response to what food type does 5-HT levels spike?

Carbs

What occurs in the phases of digestion / eating in terms of insulin?

Cephalic: -anticipate food = P.ANS activated & via vagus nerve, B-cells of the pancreas are stimulated & release Insulin -high insulin = lower the BG, brain senses this & triggers eating Gastric: -gastrointestinal hormones, like CCK = stimulate release on insulin Substrate: -nutrients absorbed, BG @ max -the increases in BG & insulin production act as satiety signal = alerts arcuate nucleus = feeding is inhibited

What does it mean, in neural terms, to be addicted to chocolate? How could chocolate elevate mood?

Chocolate is a sugary food that releases carbs into the bloodstream, thereby increasing tryptophan AA levels, and increasing the amount of brain 5-Ht = enhance your mood In terms of addictive behavior, it may activate dopaminergic neurons, acting as a reward that will reinforce the behavior of chocolate eating...creating an addiction

How does cocaine & amphetamine act as CNS stimulants? How do cocaine and amphetamine differ in their specific mechanism?

Cocaine & Amphetamine block the natural catecholamine reuptake @ DA and NE axon terminals. -causes DA and NE to be left in synaptic cleft for longer = enhanced sympathomimetic effects Cocaine: -target DA reuptake selectively Amphetamine: -targets DA & NE reuptake, and stimulates DA release

Why is it that cocaine & amphetamine typically cause psychological dependence & addiction ?

Cocaine & Amphetamine both impact / involve the dopaminergic modulatory systems (SN + VTA) -The VTA is involved in the Mesolimbocortical DA Pathway that are involved in rewarding adaptive behavior...when you short-circuit this system, it will lead to the reinforcement of addictive behaviors!

Many have accidentally killed themselves by taking large quantities of cocaine. Usually cause of death is heart failure. How do you explain peripheral actions of cocaine?

Cocaine is an sympathomimetic stimulant that acts to inhibit the reuptake of dopamine, thus allowing it to remain in the synaptic cleft longer and extending its effects. --> In acting as a sympathomimetic stimulant, it will increase BP and heart rate = Increased heart rate causes an increased need of oxygen, but with enhanced BP and narrowing of blood vessels...the need for more O2 is highly limited and can lead to cardiac arrest.

What feature of cortisol allows the HPA axis to function as a negative-feedback loop?

Cortisol is a steroid hormone, so it is "fat loving" and can pass through the blood-brain barrier. -with this ability, it can travel to the hypothalamus and directly inhibit further CRH (corticotropin-releasing hormone)! -it also travels to the anterior pituitary where it inhibits the production of corticotropin / adrenocortiotropic-releasing hormone (ACTH)

What is the function of Cortisol? What is it produced by?

Cortisol is the steroid hormone that is released by the Adrenal Cortex in response to stress. The HPA axis coordinates the release of cortisol from the adrenal cortex. Cortisol mobilizes E reserves (providing glucose) & suppresses immune system (save E) to prepare to handle stress

What is the target of Deep Brain Stimulation?

DBS targets the anterior cingulate cortex --> stimulating the anterior cingulate cortex = decreased activity & calmness, relief from depression

Between meals, when fasting, what state is this? What is happening?

Fasting state = Postabsorptive State In the Postabsorpative state, glycogen & triglyceride stores are broken down to keep providing body w/continuous supply of E The molecules are used for cell metabolism: -glucose for all cells -fatty acids & ketones for all cells, except neurons This process of breaking down the complex macromolecules is catabolism / catabolic metabolism

What is the mental disorder caused by T.Pallidum?

General Paresis of the Insane

What is Ghrelin & how does it function?

Ghrelin = a peptide hormone that is contained in the stomach & released when the stomach is empty Ghrelin stimulates appetite & food consumption by activating the orexigenic hormones of the acruate nucleus = NPY & AgRP Ghrelin also increases DA release from the VTA (enhancing the need/the motivation to get food)

How do Hallucinogens differ from CNS stimulant drugs?

Hallucinogens (LSD, psilocybin, mescaline) = target serotonin receptors / are serotonin agonists CNS Stimulants = cocaine, amphetamine, inhibit reuptake of DA and NE -different mechanism, different NT synapses targeted

What are Hallucinogens? What are some common ones, and how do they functions?

Hallucinogens = form of psychoactive drug Ex) LSD, Psilocybin, Mescaline Hallucinogens work by targeting Serotonin (5-HT) receptors! -They act as a serotonin agonist!

What are the hormones released by the parvocellular neurosecretory cells of the hypothalamus called? How do they travel?

Hypophysiotropic Hormones Travel via the Hypothalamo-pituitary portal circulation to reach the anterior pituitary

Where would you find the Sympathetic preganglionic axons?

In the intermediolateral gray matter of the SC -thoracic & lumbar regions

What is Insulin & what is it's function?

Insulin = a hormone released into the blood by the B-cells of the Pancreas (B-cells are activated the parasympathetic N.S which was turned on by the nucleus of the solitary tract) Importance: -Glucose transportation into other cells requires insulin (not neurons tho) -acts as a transported molecule for glucose (which all cells need!) Blood glucose levels & insulin levels are reciprocal to each other -high BG = low insulin -low BG = high insulin

What is true of the Enteric NS's ability to function independently?

It does function pretty independently! -It can function w/o the spinal cord or brain! -It contains sensory neurons, motor neurons & interneurons so that it can carry out reflexes and act as an autonomous integrated system

When is the parasympathetic nervous system used? What does is cause?

It is used for long-term survival. It is antagonistic to the sympathetic N.S & is used to restore the body's normal functions. Causes: slowed heart rates, decreased blood pressure, increased digestion Controls = Digestion, growth, immune response, E storage = the core things that need to be done all the time!

How does the Hypothalamus communicate with the Posterior Pituitary?

It sends neurohormones to the PP via it's Magnocellular neurosecretory neurons *think magnocellular, bc the posterior pituitary is in the back, the cells need to be bigger in order to reach it...

What was Kapp's Rabbit Experiment & how did this represent the role of the amygdala in fear?

Kapps Rabbit Exp: Kapp used *classical fear conditioning* to get rabbits to associate one tone w/painful shock & other as benign tone Before conditioning, the central nucleus of the amygdala = no response to tones After conditioning = neurons in central nucleus of the amygdala responded greatly to shock-tone & not at all to benign one Conclusion = The Amygdala, specifically the central nucleus, is conditioned / learns to respond viscerally (heart rate & BP increase) to feared stimuli

What is the neural circuit for learned fear?

Key players: -basolateral nuclei of amygdala -central nucleus of amygdala -hypothalamus, periaqueductal gray matter of brain stem, + cerebral cortex 1. Basolateral nuclei receive the fear-invoking sensory info (e.g. shock / loud noise) 2. Basolaternal nuclei send axons to the central nucleus 3. Synaptic changes in the Central nucleus w/association to painful stimulus = strengthens synaptic resp -Central nucleus efferents project to the hypothalamus, where the ANS is activated -Central nucleus projects to periaqueductal gray matter in brain stem = trigger somatic motor system / behavior -The Basolateral also sent the sensory info to the cerebral cortex, where the emotional experience is processed (e.g. unpleasant feeling)

What is Kluver-Bucy Syndrome? What is it caused by?

Kluver-Bucy Syndrome is caused by the bilateral removal of temporal lobes / temporal lobectomy (seen in monkeys) Consequences: -impaired visual recognition (using mouth to identify obj) -increased sex interest *Significant decrease in fear & aggression -flattened emotions -monkey = allow to be pet & interact humans, approach animals that they normally fear

What is the action of LSD?

LSD = serotonin agonist & Hallucinogen! -It targets presynaptic terminals of neurons in the Raphe Nuclei to inhibit firing of 5-HT neurons -Overall effect = reduced outflow of serotonergic diffuse modulatory system --> Serotonin = an inhibitory NT

What is the function of the lateral zone in the hypothalamus in terms of eating?

Lateral Hypothalamus = Motivation of feeding behavior. -Lesions in lateral zone = reduce feeding -Stimulation in lateral zone = increase feeding

What Hypothalamic region is associated with Predatory Aggression?

Lateral Hypothalamus stimulation causes predatory aggression: This is the "Silent Biting Attack" = no dramatic gestures of aggression or threats, the cat just moves in swiftly and bites the rat @ its neck

What is another name for the Submucous Plexus? (enteric NS)

Meissner's Plexus

What drugs actions are considered parasympathomimetics? What is an example?

Mimic parasymp activation -promotes muscarinic actions of ACh OR -inhibits actions of NE Ex) Propanolol = antagonist of B-adrenergic receptor for NE = inhibits Symp NS -causes lowered heart rate & BP *its a beta-blocker used to lower BP*

What is the bio theory behind affective disorders?

Monoamine Hypothesis for mood disorders: -Mood disorders cause by deficit in Monoamines = DA, NE, and 5-HT Reserpine = drug that depletes NE & DA, + 5-HT by interfering w/loading into synaptic vesicles = severe depression Monoamine Oxidase (MAO) inhibitors = increase mood, prevent destruction of NE, 5-HT, and DA

What are the drugs targeted for affective disorders?

Monoamines: NE & 5-HT Tricyclic Compounds, MAOs, SSRIs, NRIs & SRIs

What will happen when circulating leptin levels are too high? What causes this increase?

More fat = more leptin 1.Leptin will travel to & activate the arcuate nucleus in the hypothalamus. 2. The activated Arcuate Hypothalamus produces peptide hormones: aMSH and CART Humoral Resp: -aMSH & CART activates the paraventricular nucleus (part of periventricular zone) -PVN triggers the Anterior Pituitary to increase secretion of TSH (thyroid-stimulating hormone) & ACTH (adrenocorticotropin hormone) - the activated thyroid gland & adrenal glands raise the metabolic rate of cells throughout body Visceromotor: -increases sympathetic resp = increase metabolic rates (achieved by the arcuate nucleus projecting to the the brain stem & ANS preganglionic neurons) Somatic Motor: -reduce feeding behavior (arcuate nucleus projects to lateral zone of hypothal)

When are the neurons of the Locus Coeruleus most activated? How might this play into its overall function in the brain?

Most activated with new, unexpected, non-painful stimuli when alert / active (more active when alert w/ new stimuli = important for Attention (being alert), Anxiety (new stimuli), Arousal (stimuli = arousal), Learning (exploring new stimuli), and Mood) Least activated when just sitting around, digesting a meal Possible Purpose = may be to increase awareness to new stimuli, increase brain responsiveness, make sensory & motor pathways more efficient

Who does the enteric NS receive innervation / input from?

Receives input from the brain via axons of the sympathetic N.S and parasympethic N.S -functions of digestions need to be changes for certain situations, e.g. in a crisis needs to be inhibited

What NT is the locus coerulus associated with?

NE / Norepinephrine

Bilateral lesions of the lateral hypothalamus lead to reduced feeding behavior. Name three types of neurons, distinguished by NT, which contribute to this syndrome.

NYP and AgRP neurons of the arcuate nucleus of the hypothal = they are oxigenic hormones, so they increase appetite. By lesions to the lateral hypothal, the NYP and AgRP neurons will be degraded, and thus a lack of appetite / feeding behavior results. MSH = oxigenic peptide that is responsible for increasing feeding behavior, and possibly coordinating motivated behavior actions. Lesions to MSH-containing neurons will cause a decrease in feeding behavior Orexin = oxigenic peptide that promotes eating, lesions to orexin-containing neurons in the hypothal will caused reduced feeding initiation and behavior.

What is the Nucleus of the Solitary Tract? Purpose?

Nucleus of the solitary tract is located in the medulla (brain stem) & is connected with the hypothalamus (its a serious of sensory nuclei in an extended compact fiber bundles, thus the name "Nucleus of the solitary (compact) tract" Purpose = another center for autonomic control! -integrates sensory info from internal organs & influences output to the autonomic brainstem nuclei (there are preganglionic ANS neurons that originate in the brain stem) -If you only had the brainstem, some ANS functions would still work pretty well!

What is the gene ob, what does it do?

Ob gene produces the hormone Leptin!

What conclusions can be drawn from the Wacker paper?

Once LSD gets onto postsynaptic receptors, a "lid" comes over the receptor so that it cannot get out! This is why LSD has long-lasting effects.

How do Orexin and MCH function together?

Orexin and MCH are both orexigenic peptide hormones produced by neurons in the lateral hypothalamus. They are complementary, e.g. orexin will promote meal invitation, while MCH will prolong the consumption

What experiment proved that there is hormone feedback bw fat cells and the brain?

Parabiosis experiment proved that the brain & adipose tissues communicated via a blood-borne hormone signal (travel in blood) Parabiosis = long-term anatomical & physiological union of animals -Performed parabiosis of normal mouse & a obese mouse lacking both copes if *gene ob* -the feeding behavior & obesity of ob/ob mice = great reduced, bc the missing hormone was replaced by adding the normal mouse blood!

What is the disease of patient S.M that was discussed?

Patient S.M had Urbach-Wiethe Disease, causing atrophy or her temporal lobes (degradation of the amygdala) -W/o her amygdala she was indiscriminately friendly & trusting -She could not effectively recognize fear (in faces)

What is the function of the Raphe Nuclei & when are it's neurons most activated?

Raphe Nuclei = diffuse modulatory center for serotonin! Function: -involved in the sleep-wake cycle & different stages of sleeping (think melatonin sounds like serotonin) Regulates: - Control of mood - Emotional Behavior - Arousal - Breathing - Temperature (for mood & emotional behavior, think of importance of SSRI's) Neurons are most activated during wakefulness, when animal is aroused & active

How do the diffuse modulatory and point-to-point synaptic communication systems in the brain differ? List four ways.

Point-to-point synaptic communication is in regards to specific sensory and motor communication. 1) Point-to-point has anatomical precision...a specified and concrete serious of synapse in order. Diffuse systems have an extended range of axonal branching and one axon can have thousands of synapses. 2) Point-to-point communication uses exclusively the synaptic cleft to create a one-to-one cell response. The diffuse system sends NTs into the extracellular fluid / extra-synaptically, so that the NT can diffuse to several neurons vs. only the one on the post-synaptic side of the cleft. 3) Point-to-point = very brief, and then NTs are removed from the cleft via uptake by auto receptors and enzymatic degradation. Diffuse systems are long-lasting...they can range from seconds to minutes & the molecules remain lingering. 4) Point-to-point communications are defined by their specific system = visual, somatosensory, auditory, gustatory, etc. They are all unique to that system. While the diffuse systems all arise from a common source at central core of brain, mostly the brain stem.

What is the brain-stem portion of the cholinergic diffuse modulatory system ?

Pontomesencephalotegmental Complex: -This is composed of the ACh-neurons in the Pons, midbrain, and Tegmentum -The ACh of this region act in coordination w/ NE & 5-HT on the dorsal thalamus to regulate excitability of the sensory relay nuclei here *Modulates sensory regions on the thalamus* -Also involved in *REM Sleep*

What is Prednisone? What possible problems does it cause?

Prednisone is a synthetic version of cortisol that is used to suppress the immune system. Prednisone = a corticosteroid When taking prednisone, it fools the brain into thinking that your body's cortisol levels are too high, so natural production of cortisol stops. If you abruptly stop taking prednisone, you are left w/o any natural or synthetic cortisol, causing Adrenal Insufficiency Adrenal Insufficiency = fatigue, muscle weakness, weight loss, decreased appetite, low BP.

What are Psychoactive Drugs? How do they work?

Psychoactive Drugs are mind-altering drugs. -They affect the CNS by interrupting chemical synapses. -Many act directly on diffuse modulatory centers --> (Locus Coeruleus / NE), (Raphe Nuclei / 5-HT), and (SN + VTA / DA)

What was the target and purpose of psychosurgery?

Psychosurgery = brain surgery to treat psych disorders -Used to create lesions on the amygdala, to create "taming effect" in ppl

How do the kidneys, the hypothalamus, and the posterior pituitary all communicate? And what is the purpose of their communication?

Purpose: to maintain blood volume & pressure When there is a drop in BP or blood volume, the kidneys will produce the enzyme "Renin", which will then promote the production of "Angiotensin II", which activates the neurons of the Subfornical organ. The Subfornical organ then directs the hypothalamus, and the hypothalamus sends neurohormones via the Magnocellular neurosecretory cells to the posterior pituitary, which is stimulated to produce Vasopressin (ADH) The increase in Vasopressin / ADH circulation, causes a feeling of thirst!

What was discovered of the Rat's self-stimulation in Milner's experiment?

Reward Pathway: VTA projects to the Medial Forebrain Bundle (MFB), which runs right through the lateral hypothalamus -Dopaminergic Pathway -Medial Forebrain Bundle = contains the nucleus accumbens, it is involved in motivated behavior Rats: -If you stimulate DA axons through Medial Forebrain Bundle = creates craving for food, does not increasing your liking -If you eliminate DA axons = removes search / motivation to get food, but does not eliminate their enjoyment of food

What are satiety signals?

Rise in response to eating, and indicate fullness

What is the function of the Substantia Nigra in terms of it's specific NT?

SN has DA neurons -SN projects to the Striatum (caudate & putanem), where voluntary movements are initiated -degradation of the DA neurons in the SN causes motor dysfunction (Parkinson's)

What triggers the hypothalamus' regulation of homeostasis?

Sensory Transduction -A regulated parameter changes & is detected by specialized sensory neurons in the periventricular zone of the hypothalamus

What is the functions of the enteric NS's sensory neurons? motor neurons?

Sensory neurons: -monitor stretch & tension of gastrointestinal walls (monitors so it can enact digestion or peristalsis) -chemical status of stomach & intestine contents (we don't want really acidic foods damaging stuff) -hormones levels in blood Motor neurons: -govern smooth muscle motility (peristalsis / food can move through body) -production of mucous & digestive secretions (make enzymes so food can get broken down) -diameter of blood vessels (widen to absorb nutrients from intestine)

LSD has a structure that is similar to what NT?

Serotonin --> thus why LSD acts as a serotonin agonist

How is serotonin influenced by eating?

Serotonin = derived from trypothophan, which increases in blood w/more carb consumption Drugs that increase serotonin = increase satiety & act as appetite suppressants

How might serotonin be involved in aggression and anger?

Serotonin Deficiency Hypothesis: -blocking the synthesis / release of 5-HT, increases aggressive behavior *5-HT1 Receptors = involved in modulating anger/aggression* 5-HT1 agonists = decrease aggressiveness 5-HT1 antagonists = enhance aggressiveness

What is sham rage / what causes it? How do you stop sham rage?

Sham Rage is caused by the removal of the cerebral hemispheres -animal = extremely violent w/ little provocation Sham = would not normally be in rage bc of that stimulus & bc it normally does not react like that when it is in a rage You can stop sham rage by cutting the *Posterior Hypothalamus! -Posterior Hypothal must be involved in expression of anger/aggression that it typically inhibited by the telencephalon that was removed

What was Shultz experiment? What did it show?

Shultz = looked @ what happens to DA neurons in monkey when given juice after flashing light -first = no resp to light, brief juice resp -w/conditioning = resp. to light, not to juice DA neurons fire with cues that predict the reward -Better than exp = fire DA -Worse than exp = inhibit DA -Exp events = no DA firing *Cues can drive your craving / wanting!

Name one way the vagus nerve can stimulate feeding behavior, and one way it can inhibit it.

Stimulate feeding behavior = the descending vagus nerve stimulates the expanding of blood vessels along intestines to absorb nutrients & also descending vagus nerve activity (ACh) causes parasympathetic innervation of the pancreas; stimulating pancreas B-cells to release insulin...this insulin causes a drop in blood sugar which drives us to eat Inhibition = ascending vagus nerve - told by gastric distention and cholecystokinin (CCK) that the body is fed & full --> the vagus nerve sends these signals to the nucleus of the solitary tract, which then inhibits feeding behavior

What happens when the Amygdala is stimulated?

Stimulation creates fear & anxiety fMRI shows that neural activity in amygdala: -more amygdala activity in response to fearful faces vs. expressionless faces -there is no diff. in amygdala activity when being showed happy or neutral faces .... this shows that the amygdala is specifically activated when person recognizes fear

What is the Hypothalamus region associated with Affective Aggression?

Stimulation of the medial hypothalamus causes affective aggression: This is the "Threat Attack / Response" form = cat will hiss, arch its back, but won't attack victim

How does the sympathies NT use differ from the parasympathetics?

Symp uses NE, which has wide-spread effects Parasymp uses ACh which has more local effects on its targets using mAChRs

Why might creating lesions in the amygdala reduce anger / aggressive outputs?

The Amygdala = involved in fear / perception of fear. It additionally influences both the hypothalamus and the VTA & Periaqueductal gray matter of the midbrain, thus playing a pretty influential role in the circuit for aggressive behavior. If the Amygdala is overactive, it may be overproducing signals to the hypothalamus & VTA & PGA, causing more anger / aggressive responses

What is the arcuate nucleus? What are it's effect?

The Arcuate Nucleus is a part of the hypothalamus that decreases appetite & increases E expenditure. Arcuate Nucleus is dense in leptin receptors: -regulates body mass -decreases appetite -increases E expenditure *Leptin & Arcuate Nucleus = key in regulating food intake, telling the body when to stop!*

What is the role of the cerebral cortex in the aggression circuits?

The Cerebral Cortex has direct influence / regulation over the amygdala, and the rest of the downstream players (Medial Hypothal, Lateral Hypothal, VTA, periaqueductal gray matter in midbrain) The Cerebral Cortex keeps emotions in check / inhibits the aggression... -Phineas Gage personality change -Sham Rage

What diffuse modulatory center is implicated with Alzheimer's Disease?

The Cholinergic Basal Forebrain Complex -this area = known to perish during Alzheimers

How does the Hypothalamus (periventricular zone) control the Anterior Pituitary?

The Hypothalamus controls the Anterior Pituitary via Parvocellular neurosecretory cells The Parvocellular neurosecretory neurons release hypophysiotropic hormones that travel via the hypothalamo-pituitary portal circulation to reach the anterior pituitary.

What are some homeostatic functions? What portion of the brain is largely in charge of homeostasis?

The Hypothalamus is in charge of maintaining homeostasis! Homeostatic Functions: -blood volume -blood pressure -temperature -blood acidity -blood salinity -blood oxygen -glucose levels --> all things we can't consciously control, but need to be optimized in order to survive

What is the Hypothalamus? And what function does it serve for the body?

The Hypothalamus makes up less than 1% of the brain's mass, but is a key portion of the brain that connects the body's endocrine system & nervous systems. Functions: -Integrates somatic & visceral responses -Maintains Homeostasis **

What is the Lipostatic Hypothesis?

The Lipostatic Hypothesis: -the brain monitors that amount of body fat, and defends this form of E storage against any changes to it -Loss of fat during starvation period = quickly gained back when exposed to normal food levels -Body weight gain via forced feeding is quickly lost once returned to normal conditions These trends indicated hormonal feedback - communication bw the adipose & the brain

What is the Locus Coeruleus? Where is located?

The Locus Coeruleus is the diffuse modulatory system for NE -it a group of noradrenergic neurons / nuclei Location: The Locus Coeruleus is a nucleus located in the pons (brain stem) & is made up of ~12,000 neurons

How is motivation influenced / controlled by neuromodulation?

The Mesocorticolimbic System in the brain is key in controlling motivation, and therefore - behavior. This pathway enhances / increases behavioral responses: -can be adaptive behaviors (food, sex, thirst) -can be maladaptive (drugs of abuse) Motivation is the driving force on behavior & changes the probability of a behavior occurring

Under what behavioral conditions are the noradrenergic neurons of the locus coeruleus active? The noradrenergic neurons of the ANS?

The NE neurons of the locus coeruleus are active when the animal is awake and active, and when it is receiving new, unexpected, non-painful stimuli from the environment. They are least active when the animal is simply sitting around quietly, not vigilant, just digesting a meal. --> Locus Coeruleus has NE is heavily connected to the neocortex = makes the brain more aware and increasingly responsive to salient (important/obvious) stimuli, speed up point-to-point transmission of sensory and motor systems --> make the more efficient. The NE neurons of the ANS are involved in the sympathetic division. They are activated in times of crisis / The Four Fs --> Flight, Fight, Fright, Sex --> They prepare the body for short-term emergencies in the Four F situations!

What is the Raphe Nuclei? Location?

The Raphe Nuclei is the diffuse modulatory system for Serotonin Nine nuclei in the brain stem: -more caudal ( more down) = in the medulla & innervate the spinal cord + modulate pain-related sensory signals (think caudal = cord) -more rostral (towards top) = in pons /midbrain + innervate brain in diffusive manner (rostral has a t, so top!)

Out of the three hypothalamus responses, which is the fastest, most effective way at correcting a disturbance in homeostasis?

The Somatic Motor Response These are motivated behaviors that are initiated by the lateral hypothalamus

What is the NT used by the postsynaptic ganglion cells of the sympathetic NS? Parasympathetic?

The Sympathetic NS uses Norepinephrine (NE), which has wide effects & spreads into blood The Parasympathetic NS continues to use Acetylcholine (ACh) which has local effects on its targets, acting via mAChRs

Why is the adrenal medulla often referred to as a modified sympathetic ganglion? Why isn't the adrenal cortex included in this description?

The adrenal medulla is referred to as a modified sympathetic ganglion bc it produces epinephrine (Adrenaline) and norepinephrine (NE) --> which act very similarly; these NT's have identical effects as the sympathetic N.S; thus why they are considered to be modified sympathetic ganglion (increases heart rate, increases BP, enhances blood flow) --> The adrenal cortex is not included in this description because it produces cortisol, corticosteroids, and aldosterone. It is primarily involved in stress responses, and metabolism. It is not always acting in the direction of the sympathetic N.S, could be more focused on digestion and low stress response

What is the purpose of the hypothalamus' control over the Anterior Pituitary? What does the communication function to do?

The connection bw the Hypothalamus & the Anterior Pituitary functions in the overall Hypothalamic-Pituitary-Adrenal Axis (HPA axis) HPA Axis function: -controls the stress response -regulates stress levels Hypothalamus (periventricular zone) Anterior Pituitary Adrenal Cortex

In what ways does the Hypothalamus control the Posterior Pituitary Gland?

The hypothalamus controls the Posterior Pituitary via large hypothalamus cells : Magnocellular neurosecretory neurons, which release neurohormones directly into the posterior pituitary's capillaries Causes the PP to release: 1. Oxytocin 2. Vasopressin

What NT is used by the preganglionic neurons of the sympathetic N.S and the parasympathetic NS?

The preganglionic neurons of both divisions use ACh / acetylcholine ACh = fast-acting & excitatory ACh binds to nicotinic ACh receptors (nAChR), creating an EPSP that triggers an AP in the postganglionic cell -nAChR = ionotropic receptor ACh also binds to muscarinic ACh receptors (mAChR), which are metabotropic GPCRs, creating slow EPSPs and IPSPs -Some preganglionic cells release neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP)

Surgical approach to reducing excessive body fat is liposuction - removal of adipose tissues. Over time, body adiposity usually returns to same value as before surgery. Why is liposuction not a permanent solution? What about gastric surgery to treat obesity?

The return of the wait is due to the lipostatic hypothalamus, which monitors the amount of body fat and defends against changes in it --> thus why after reducing adipose, body weight usually returns right after when normally exposed to food. Gastric surgery = more long-term / effective bc gastric surgery changes the gastrointestinal hormones produced in a way that reduces hunger and appetite, and increases satiety / fullness.

Kluver-Bucy Syndrome vs. Urbach-Wiethe Disease:

They both are result from the degradation of the amygdala Kluver-Bucy = in monkeys Urbach-Wiethe Disease = in humans, seen in patient S.M

What drugs are considered Sympathomimetic?

They mimic Sympathetic N.S activation -promote actions of NE OR -inhibit muscarinic actions of ACh

Is the Mesocorticolimbic Pathway more coordinated towards wanting, or towards liking? How do we know this?

This DA pathway is more centered around "wanting & craving", but not overall "liking" DA blockers = decrease efforts to seek out food, aka lowers the rat's "wanting/craving" for food; but did not decrease overall "liking" - if you give rat food it will still like & enjoy it DA stimulation = increases seeking and "wanting", but does not affect "liking"

What is the Mesocorticolimbic Pathway?

This pathway is involved in one of the brain's diffuse modulatory systems for dopamine (DA). 1. Begins in the Ventral Tegmental Area (VTA) (part of midbrain) 2. VTA projects to the nucleus accumbens, which is in the basal ganglia & part of the limbic system 3. VTA also projects to the frontal cortex Functions in learning & motivation, the "reward" pathway, and is involved in some psych disorders

Where do the preganglionic axons from the Sympathetic NS emerge from?

Thoracic and Lumbar regions -sympathetic preganglionic neurons lie in the intermediolateral gray matter of the SC

What is learned fear? How is this related to the amygdala and fear?

Through socialization of painful experiences, we learn to avoid specific behaviors for fear of being hurt -This is why you don't see ppl going around touching hot stoves all the time! Amygdala: -synaptic changes in the amygdala are important in forming memories for emotional events -amygdala neurons "learn" to response to stimuli associated w/pain & after learning, the stimulus evokes a fearful response! --> Amygdala basically regulates the conditioned response / learned fear of a fearful stimulus

T/F LSD is better at binding to serotonin receptors that natural serotonin.

True, new studies show that LSD actually supersedes natural LSD binding in cortical areas where perceptions are naturally formed & interrupted

What areas are involved in the cholinergic diffuse modulatory system?

Two major systems: 1. Basal Forebrain Complex 2. Brainstem

What is Urbach-Wiethe Disease? What is it caused by?

Urbach-Wiethe Disease: Caused by bilateral degradation of Amygdala; the disease creates atrophy via temporal lobe Patient S.M: -removal of her amygdala caused her to become indiscriminately friendly & trusting -when showed fearful faces, she rarely identified them as "fear" (she didn't look @ ppls eyes when she assessed their mood) = possible that fear is a two-way interaction bw the amygdala & visual system

When is the Sympathetic N. S used? What does it cause?

Used in crisis; for short-term emergencies! Four F's = Fight, Flight, Fright, Sex Causes increased heart rate, elevated BP, depressed digestive functions, mobilized glucose reserves

What is the function of the Ventral Tegmental Area in terms of its specific NT?

VTA = contains DA-neurons DA neurons in the VTA project to the Frontal Cortex & the Limbic System (nucleus accumbens in the basal ganglia) (Projection = Mesocorticolimbic DA System) Functions: -learning and motivation -involved in the "reward" system that assigns value & reinforces adaptive behaviors -implicated in psych disorders

What is the significance of having motivation? Why do we need it?

Voluntary movements are incited to occur / *motivated*, in order to satisfy a need Internal Motivation is the driving force on our behaviors! -we have abstract motivation = the "need" to go sailing -we have concrete motivation = the need to go pee Why do we need it? -it is critical for maintaining homeostasis & surviving --> eating, drinking, repro The probability of a behavior is dependent on the level of driving force to perform that behavior Motivation is *required* for a certain behavior, but it does not guarantee the behavior (motivated to go pee, but have condition where you physically can't)

Battlefield trauma victims who have lost large volume of blood often express craving to drink water...Why?

When a person experiences a large drop in either blood volume OR pressure --> this causes communication bw the kidneys and the hypothalamus: -Kidneys will sense drop in BP or blood volume and produce the enzyme Renin, this will in turn come to up-regulate the production of Angiotensin II, which then excites neurons of the Subfornical organ, which directs the hypothalamus to increase the production of Vasopressin / Anti-diuretic hormone (ADH) via the posterior pituitary, which causes the feeling of thirst --> The PP is directed by the periventricular hypothalamus via Magnocellular neurosecretory cells --> Vasopressin / ADH = hormones produced by the posterior pituitary gland, as directed by the hypothalamus --> Vasopressin regulates blood volume and salt concentration -This is an important Ex of how, to some extent, the kidneys control the brain

aMSH and CART are considered.....

anorectic peptides -they are peptide hormones that diminish appetite (anorectic sounds like anorexia)