Biopsychology Exam 3

endogenous rhythms

Internal biological rhythms independent of external cues. (biological clock)

zeitgeber

a stimulus (ex: the light of dawn) that resets the biological clock

Suprachiasmatic Nucleus (SCN)

area of the hypothalamus in which neurons generate their own circadian rhythm

damage to SCN

causes circadian rhythms to disappear

isolated SCN neurons

still show rhythmic electrical activity

Hamster experiment (and the SCN)

Transplanted SCNs dictate circadian rhythms in the host

Retinohypothalamic Path

neural pathway from retina to SCN

Melanopsin

ganglion cells in retinohypothalamic pathway contain _______

Ganglion cells with melanopsin respond . . . .

slowly to light (mostly short wavelength/blue)

PER and TIM

proteins that build up during the day then promote sleep

Light activates a chemical that breaks down ______

TIM

Pineal Gland

activity modulated by SCN

Melatonin is released by . . .

pineal gland

Melatonin production increases . . .

2-3 hours before sleep

polysomnograph

combination of EEG (electroencephalogram) and eye movement tracking

Stage 1 (brain activity)

Theta waves, high brain activity, drifting to sleep

Stage 2 (brain activity)

Theta waves, K complexes, sleep spindles, deep relaxation

SWS (Slow Wave Sleep S3-4)

Delta waves, difficult to wake, non-REM dreams

REM Sleep

Sawtooth waves, rapid eye movement, difficult to wake, most dreams

Sleep Cycles

90 minutes each, 4-5 per night

Pontomesencephalon releases . . .

ACh, glutamate, dopamine

Pontomesencephalon maintains . . .

arousal

Pontomesencephalon axons project to . . .

forebrain

Locus Coeruleus releases . . .

Norepinephrine

Locus Coeruleus responds to . . .

emotional events, enhanced memory

Locus Coeruleus axons project . . .

throughout cortex

tuberomammillary nucleus

releases histamine, promotes arousal

Lateral and Posterior Nuclei

release orexin to promote wakefulness

Basal Forebrain

releases ACh, projects to thalamus

GABAergic neurons (during sleep)

MORE active

REM sleep increases activity in . . .

pons, limbic system, parietal cortex, temporal cortex

REM sleep decreases activity in . . .

primary visual cortex, motor cortex, dorsolateral prefrontal cortex

PGO waves

pons-geniculate-occipital, high amplitude electrical potentials during REM sleep

Ventral medulla

GABAergic pathway here promotes REM sleep

ACh

important for REM sleep

Serotonin and Norepinephrine

interfere with REM

Energy Conservation

sleep theory supported by decreased body temp, muscle activity, hibernation

brain restoration

sleep theory supported by irritability, impaired performance when tired

Memory (sleep theory)

better memory, better new info intake after sleep, hippocampus functions similar to waking

brain development

function of REM sleep

strengthening memories

function of REM sleep

Activation-Synthesis Hypothesis

brain is attempting to make sense of information during dreams, dreams initiated by PGO waves, waves activate cortex, cortex tries to make story

Neurocognitive Hypothesis

Dreams = thinking under unusual conditions, memories create spontaneous activity

Defense Activation Theory

dreaming activates visual cortex to prevent cortical reorganization

homeostasis

active physiological process that keeps variables within a set range

negative feedback

processes that reduce deviation from set point (ideal range)

allostasis

body anticipates needs depending on situation

most energy is spent . . .

on basal metabolism

fight or flight capability

benefit of high body temp

reasons for body temp

energy, proteins denaturing, reproductive cells

POA/AH (Preoptic Area and Anterior Hypothalamus)

brain area that responds strongly to temperature

norepinephrine (when hot)

is inhibited, vasodilation, lower metabolism

ACh (when hot)

increased activity, sweating

norepinephrine (when cold)

increased, vasoconstriction

fever (steps)

infection, white blood cells/cytokines, vagus nerve, hypothalamus, increased prostaglandins, fever

osmotic thirst

caused by osmotic pressure when there is a greater concentration of extracellular solutes

osmotic receptors (location)

OVLT and SFO

osmotic thirst pathway

osmotic receptors, hypothalamus, posterior pituitary, vasopressin, vasoconstriction (water retention)

hypovolemic thirst

caused by loss of fluids

hypovolemic thirst (receptors)

baroreceptors (blood vessels) and receptors in kidneys

osmotic thirst pathway

osmotic receptors, lateral preoptic area (hypothalamus), drinking behavior

hypovolemic thirst pathway

baroreceptors, kidneys release renin, angiotensin II, constricts blood vessels, stimulates SFO

hypovolemic thirst pathway

baroreceptors, pituitary gland, vasopressin

distention of stomach stimulates . . .

vagus nerve

distention of duodenum releases . . .

CCK

insulin

short term hormone, regulates blood sugar levels by facilitating glucose uptake

glucagon

short term hormone, raises blood glucose levels, antagonistic to insulin

leptin

long term hormone produced by adipose (fat) cells that regulates appetite

ghrelin

long term, hunger hormone secreted by empty stomach

type I diabetes

insulin is not produced

type II diabetes

not enough insulin or insulin doesn't work

GLP-1 (definition)

glucagon-like peptide 1

GLP-1 (function)

naturally occuring, binds to GLP-1 receptors, short term satiety signal produced by intestinal cells

semaglutide (ozempic) function

agonist of GLP-1 receptors

GLP-1 and substance disorders

GLP-1 has shown promising ability to help with alcoholism and substance abuse

NAc (GLP-1)

nucleus accumbens, motivation, reward

BNST (GLP-1)

bed nucleus of stria terminalis, stress, anxiety, reward

Vhipp, LDT, NTS, (GLP-1)

reward-related behaviors

arcuate nucleus (contains)

hunger and satiety cells

PVN (Paraventricular Nucleus)

receives input from Arcuate Nucleus, if excited it inhibits LH

LH (Lateral Hypothalamus)

releases orexin to facilitate feeding behavior

hunger/satiety brain mechanism

arcuate nucleus, PVN excited, PVN inhibits LH, orexin stops

hypothalamus hunger circuit

ghrelin/glucagon/taste, arcuate nucleus, GABA/NPY/AgRP, PVN, LH, orexin

hypothalamus satiety circuit

CCK/Glucose/GLP-1, arcuate nucleus, Glutamate/POMC/CART, PVN, LH inhibited

VMH (Ventromedial Hypothalamus)

a brain region that depresses hunger when activated

damage to VMH causes . . .

overeating, weight gain, frequent meals

hypoglycemia

low blood sugar

hypoglycemia (with diabetes)

caused by treatment, too much insulin/medication, low food intake

hypoglycemia (without diabetes)

caused by insulin overproduction, hormone imbalances, alcohol abuse

prader-willi syndrome (caused by)

chromosome 15 mutations

prader-willi syndrome (symptoms)

low muscle tone, hyperphagia, OCD, learning disability

prader-willi syndrome (cause of hyperphagia)

hypothalamus dysregulation, releases more orexin, increased ghrelin

binge eating disorder (symptoms)

binges, lack of control over eating, once/week for 3 moths

binge eating disorder (biological factors)

genetic risk, increased ghrelin, NAc responds stronger to food

bulimia nervosa (symptoms)

binging, purging, strict diet, excercise

bulimia nervosa (biological factors)

genetic risk, increased ghrelin, low serotonin

anorexia nervosa (symptoms)

low food intake, low body weight, fear of weight gan

anorexia nervosa (biological factors)

genetic risk, increased amygdala activation, cortical thickness

sex chromosomes

23rd chromosome pair that determine sex

sexual differentiation (starts)

7-9 weeks