PSY 210 Exam 3 Learning Outcomes

Mercer University

Endogenous rhythms

internal mechanisms that help organisms anticipate environmental changes

biological clock 

zeitgebers

stimulus that sets/resets the biological clock

Social stimuli is not enough to reset circadian rhythm

suprachiasmatic nucleus

Part of the hypothalamus

Neurons generate their own circadian rhythm!

retinohypothalamic path 

pathway from retina to the SCN

Special ganglion cells contain melanopsin

Respond directly to light

Slow response to light

Respond mostly to short wavelength (blue)

Exposure to light late in the day can phase-delay circadian rhythm

PER genes

shorter circadian rhythm

TIM genes

regulate circadian rhythm stability

Melatonin

SCN modulates the activity of other brain areas including the pineal gland

Pineal gland releases melatonin

Melatonin production increases 2-3 hrs before bedtime

Taking melatonin earlier in the day will phase advance circadian rhythm

Stage 1 of sleep

Theta waves 

higher brain activity 

drifting off to sleep, muscle relaxation begins 

Stage 2 of sleep

theta-like waves

k complexes and sleep spindles

deep relaxation 

Stage 3 and 4 of sleep

about 20% of sleep

difficult to wake up out of this stage

non-REM dreaming usually associated with slow waves

REM sleep

About 20-25% of time asleep

Difficult to wake up

Rapid eye movements and muscle atonia

Most dreaming

Sleep Cycles 

One sleep cycle is about 90 min

About 4-5 cycles per night

Pontomesencephalon neurotransmitters realesed

releases acetylcholine, glutamate, or dopamine 

Locus Coeruleus neurotransmitter released to promote wakefulness 

releases norepinephrine

Tubermammillary nucleus neurotransmitter released to promote wakefuless

releases histamine

Later and posterior nuclei neurotransmitter released to promote wakefulness

releases orexin

basal forebrain neurotransmitters released to promote wakefulness

releases acetylcholine

Key neurotransmitter and activity changes associated with sleep

GABAergic neurons 

Brain regions with increased activity during REM 

PONS

Limbic System 

Parietal Cortex

Temporal Cortex

Brain region with decreased activity during REM

Primary Visual cortex

motor cortex

dorsolateral prefrontal cortex

PGO waves

pons-geniculate-occipital

High amplitude electrical potentials

Pons→LGN→Occipital cortex

neurotransmitters and regions involved in REM

Ventral Medulla-GABAergic pathway

Acetylcholine is important

Energy Conservation

Decreased body temp (1-2 degrees)

Decreased muscle activity

Hibernation

Restoration of the brain/body

Sleep deprivation causes a lot of problems...

Irritability

Impaired cognitive performance

Impaired concentration

Increased risk for accidents (psychomotor function)

Memory

Sleep deprivation = worse performance on memory tasks

Better memory of new information after sleeping

Theories as to why we have REM sleep – development, memory

brain development- get less REM aleep as we age

Strengthening memories- memory consolidation happens during REM

Activation-Synthesis Hypothesis

Brain attempts to make sense of sparse and distorted information

Dreams are initiated by PGO waves

PGO waves activate random areas of the cortex

Cortex combines the random neural activity and tries to make a story out of it

Neurocognitive Hypothesis

Dreams are thinking that takes place under unusual conditions

Dreams begin with spontaneous activity related to recent memories

Activity in visual cortex and limbic areas during sleep may relate to visual aspect of dreaming

PFC activity is suppressed – maybe allowing for more creativity, contributing to forgetting dreams

Defensive Activation Theory

Dreaming activates the visual cortex to prevent cortical reorganization

Suggest that PGO waves may be triggered when visual cortex activity decreases too much

Looked at known data from several different primate species

Amount of time spent in REM sleep correlates with measures of plasticity

Plasticity and REM sleep increase the more closely related the species is to humans

ERP

Event-Related Potential, a measured brain response resulting from a specific sensory, cognitive, or motor event.

sleep deprivation on selective attention?

negatively impacts selective attention, leading to reduced focus and increased distractibility.

Homeostasis

physiological process that keeps biological variables within a set range

Active process!

Allostasis

the body anticipates needs depending on situation

Preemptive compensatory mechanism

POA/AH function

Integrates information from skin, organs, and hypothalamus

Has the strongest response when both the skin and internal body is cold or hot

what happens when we’re too hot and need to cool down

Inhibit norepinephrine – vasodilation, reduce basal metabolism

Increase acetylcholine activity – sweating

when we’re too cold and need to warm up

Stimulation of brain stem motor areas shivering

Increase norepinephrine vasoconstriction

Steps your brain/body takes to generate a fever

1. Infection enters the body (e.g., virus)

2. White blood cells release cytokines

3. Vagus nerve is stimulated → sends message to hypothalamus

4. Increase of prostaglandins

5. Fever (increased set point)

Cause of osmotic thirst

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

What detects changes in osmotic pressure?

Receptors around 3rd ventricle detect sodium content and osmotic pressure

OVLT and SFO

Pathways that help relieve osmotic thirst

Hypothalamus → Posterior Pituitary Secretes Vasopressin → Vasoconstriction

Lateral Preoptic Area→Drinking behavior 

What is the best thing to drink to relieve osmotic thirst?

Water or electrolyte drink is the best choice.

Cause of hypovolemic thirst

caused by losing significant amount of body fluid (low volume)

What detects changes in overall fluid volume/pressure?

Baroreceptors

Pathways that help relieve hypovolemic thirst

baroreceptors detect decreased blood pressure → kidneys release renin → angiotensin 2 is produced → constricts blood vessels

What is the best thing to drink to relieve hypovolemic thirst?

blood or electrolyte beverage

Hunger and Satiety Signals from digestive system

Ghrelin and leptin

Insulin

enables glucose to enter cells

Glucagon

regulate flow of glucose

in the bloodstream, promoting glucose release from the liver.

GLP-1

naturally occurring

short-term signal of satiety produced in intenstinal cells 

actions are opposite of glucagon 

Leptin

produced by fat cells

higher levels cause lower hunger and promote activity

low levels promote eating 

Ghrelin

secreted by stomach 

acts on the hypothalamus to increase food intake 

Hypothalamus areas involved in hunger & satiety

Arcuate nucleus

Paraventricular nucleus (PVN)

Lateral Hypothalamus (LH)

Arcuate Nucleus

Hunger cells

Satiety Cells

Paraventricular Nucleus (PVN)

receives input from arcuate nucleus

when excited, it inhibits the LH

Lateral Hypothalamus (LH)

Releases orexin to facilitate feeding behavior 

How hunger & satiety signals (insulin, glucagon, etc.) will affect the cells in the

arcuate nucleus

What neurotransmitters and neuropeptides are released by hunger

Ghrelin

Glucagon

Taste input 

What neurotransmitters and neuropeptides are released by satiety cells

Leptin 

Insulin

CCk

Glucose

GLP-1

How the activation of hunger cells alters the activity of the PVN and the LH

Hunger cells use inhibitory neurotransmitters and stop the hunger circuit

Use of GABA, NPY, and AgRP

Creates the release of orexin

How the activation of satiety cells alters the activity of the PVN and the LH

Use excitatory neurotransmitters on PVN

Use inhibitory Neurotransmitters for LH

stops the release of orexin

What will high vs low orexin release from the LH do

High orexin levels stimulate appetite and increase food intake

while low orexin levels reduce hunger and decrease eating behavior.

Function of ventromedial hypothalamus (VMH)

output inhibits feeding behaviors

damage to this area causes overeating and weight gain

type 1 diabetes

insulin not produced

type 2 diabetes

not enough insulin produced and/or insulin doesn’t function typically

Hypoglycemia

low blood sugar

with diabetes can be caused by treatment

without diabetes can be caused by overproduction of insulin 

Prader Willi syndrome

genetic disorder caused by mutations on chromosome 15

low muscle tone in infancy

learning disabilities

Obsessive compulsive behavior 

Hyperphagia: constant hunger/drive to consume food 

Binge eating disorder

Binges of eating a lot of food in a short period of time

feeling a lack of control

increased ghrelin production NAc activates more strongly 

Bulimia nervosa

Alternate between binging and strict diet ‘

at least once a week for 3 months 

low levels of serotonin and increased ghrelin 

Anorexia nervosa

significant and persistent reduction in food intake

intense fear of gaining weight

increased activation of amygdala

increased cortical thickness

SRY Gene

sex-determining gene on y chromosome

Female pattern of development for reproductive organs

Lack of SRY gene and androgens cause gonads to become ovaries

Wolffian ducts degenerate

Mullerian ducts develop into fallopian tubes, uterus, upper vagina

Male pattern of development for reproductive organs

Androgens cause Wolffian ducts to develop into seminal vesicles and vas deferens

Testes produce Mullerian inhibiting hormone (MIH) which causes Mullerian ducts to degenerate

Sex hormones 

androgens

estrogens 

progesterogen 

3 ways hormones can have effects on cells

1. Bind to membrane receptor

2. enter cells, activate proteins in cytoplasm

3. bind to receptors that bind to dna

Organizing Effects

long-lasting, structural effects 

Activating effects

temporary effects reflecting current hormone levels

Sex differences found in brain structure

Males have higher total brain volume

females have more gray matter 

males have more white matter 

How alpha-fetoprotein relates to brain feminization and masculinization in rodents

binds to estradiol in females 

in males testosterone crosses BBB

Sex differences in play behavior

males tend to prefer playing with cars, balls, roughhousing

females tend to prefer calmer and cooperative play

Hypothalamus → pituitary → gonad axis (what hormones are released by each in males and females)

males release GnRH

luteinizing hormone released from anterior pituitary

Male hormone cycle

follows circadian cycle

testosterone levels tend to increase in morning and decrease throughout day

female hormone cycle

Follows a monthly cycle

Sex bias 

favoring one sex over another in research

sex omission

lack of reporting sex in research

Hormones and brain areas involved in parenting behaviors in females

prolactin 

oxytocin 

Estradiol

Hormones and brain areas involved in parenting behaviors in males

prolactin

oxytocin

Prairie vs meadow voles

Meadow voles are hoes

Prairie voles are family driven

Intersex individuals

Individuals possessing both male and female biological characteristics.

Congenital adrenal hyperplasia (CAH)

overdevelopment of adrenal gland

disrupted negative feedback cycle between adrenal glands and brain 

less severe effects in males

Females with CAH

varying degree of reproductive organ and brain masculinization 

play with boy toys more than girl toys

have better spatial and mechanical skills than other females in early childhood

Androgen insensitivity Syndrome (AIS)

lack of androgen receptors in males 

people with complete AIS often Raised as girls, partial AIS often raised as boys 

males have higher rates of anxiety and depression 

SRY gene mutatation on XY male 

missing/severe mutation: complete lack of masculinization 

less severe mutations: less masculinization 

SRY gene mutation on XX female

translocated gene

masculinizes females

usually develop testes but are infertile

Turner Syndrome

underdevloped ovaries

short stature

learning disabilities

reduced gray matter volume in parietal lobe

Klinefelter Syndrome

underdeveloped testes, low testosterone production

tall stature

deficits in attention and working memory

reduced gray and white matter

Triple X Syndrome

can be delayed or early puberty 

delayed speech and language development 

higher rate of mood disorders 

smaller gray matter volume in hippocampus and amygdala