PSY 256 Exam 4

endogenous rhythms

biological rhythms in the brain

are dependent on both external and internal ques

external endogenous cues

seasonal light/dark patterns

activate make the endogenous system

internal endogenous cues

endogenous rhythms (brainactivity)/biological makeup

activate the endogenous systems

circannual rhythm

around 1 year long- daylight savings stuff

circadian rhythm

around 1 day long, not just sleep

includes hunger and thirst cues, body temp, urination, hormonal secretion, sensitivity to drugs

zeitgerber

stimuli that resets the circadian rhythm, like sunlight, exercise, arousal, and body temp

what changes our biological clocks?

daylight savings, jetlag, shift work (sleeping at different times)

can eventually be shifted, but not instantly.

what is a chronotype?

morning vs. night people

determined by age, genetics, and environment

superchiasmic nucleus

endogenous system

main drivers for sleep and body temp rhythms; produces cells that release chemicals in 24hr pattern

within the hypothalamus, on top of the optic chasm (X).

retinohypothalamic path

endogenous system

path from experiencing light to body releasing appropriate chemicals.

ganglion cells take in light which is sent to the superchasmic nucleus allowing us to respond to day/night

PER and TIM genes

endogenous ssytem

protein concentrates oscillates over a day telling us when to sleep/ wake

pineal gland

endogenous system

produces melatonin, releases more around bedtime

what is sleep?

a **specialized state actively produced** by the body and brain.

different from all other levels of consciousness

awake, relaxed state

alpha waves

stage 1

irregular, low voltage waves

stage 2

k complex and sleep spindle waves

stage 3

many slow, large amplitude waves

stage 4

few slow, large amp. waves

REM sleep

similar to stage 1 + paralysis

how do we go through the sleep stages?

like an hourglass

1, 2, 3, 4, 3, 2, 1, REM, 1, 2…

when do we experience more REM vs. deep sleep?

more deep sleep- 1st 1/2 of the night

more REM- 2nd 1/2 of the night

reticular formation and sleep

ascending fibers from the midbrain to the forebrain,

involved in arousal/inhibition

inhibition- GABA

arousal- acetylcholine and glutamate

inhibition in the reticular formation

GABA (slows the brain)

arousal in the reticular formation

acetylcholine and glutamate (wakes the brain)

locus coeruleus and sleep

within the pons,

responds to meaningful events/stimuli (like hearing your name), emotional arousal

responds to caffiene, too

norepinephrine

hypothalamus and sleep

important for wakefulness and sleep

hystamine (+) enhances arousal and alertness

orexin/hypocritin- staying awake

hystamine (+)-

hypothalamus, enhances arousal and alertness

orexin/hypocritin-

hypothalamus,, staying awake

increased activity during REM in

pons (triggers REM onset)

limbic system

parietal cortex

temporal cortex

\*\*think dreaming senses, we talk to others, have emotins, and feel things

decreased activity during REM in

visual cortex

motor cortex

dorsolateral prefrontal cortex

\*\*we cannot see or move, and our dreams are not logical

PGO waves

REM sleep characteristic

tell researchers when we are in REM

pons geniculate (thalamus) occipital waves that tell us about brain activity

functions of sleep

energy conservation, decrease metabolism, cellular maintenence, reorganizing synapses, and strengthening memories

activation synthesis hypothesis

**brain creates a story with random brain waves to make sense of them**

many brain regions are active, and the brain creates a story to make sense of it

\*\*What I believe

neurocognitive hypothesis

**dreams orig-inate mostly from the brain’s own motivations, memories, and arousal. The stimulation often produces peculiar results because it does not have to compete with normal visual input and does not get organized by the prefrontal cortex.**

components of emotions

cognitive- awareness of experience

action/behavior

feelings- internal experience

physiological response- emotion changes

autonomic NS and emotions

ParaSympatheticNS and SympatheticNS control our physiological response to stimuli

SympNS and emotions

activates emergency response- heart rate

ParaSympNS and emotions

deactivates emergency response, preserves energy

PRESERVES, PARASYMP.

james lange theory of emotions

event→ appraisal/cognition→ action→ emotion/feelings

we give labels to the response we have to stimuli, which we call emotions. \*\*we take action (behavior) then feel something about it

pure autonomic failure

lack of physical reaction, but can still feel emotions

in favor of james lange theory

botox

paralyzed face muscles, less emotional response

in favor of james lange theory

somatosensory cortex damage

physiological response but cannot feel emotions

not in favor of james lange theory

prefrontal cortex damage

weak autonomic response but still feel emotions

in favor of james lange theory

pure autonomic failure and botox

not in favor of james lange theory

somatosensory cortex and prefrontal cortex damage

physiological arousal

generic to all emotions- LOOKS THE SAME

not suffient to produce the emotion, but helps

different emotions are not expressed uniquely in the cortex

limbic system (amygdala) and emotions

traditionally linked to emotions w/ the active cortex

learned fears

connects to the hypothalamus and endocrine system

controls breathing, heartrate, and tells us to avoid situations

Eckman

certain emotions are universally recognized

experiment showing people pics of faces and asking what emotion they felt

dimensional emotional model

aroused, unaroused, pleasant, and unpleasant plain categorizing all emotions.

activation of emotions

BAS

left brain in frontal and temporal lobes

happiness, anger

inhibition of emotion

BIS rIIIIght

right brain in frontal and temp lobes

fear, disgust

inhibits unnessecary processes/actions to help us decide what to do. then, response is activated.

functions of emotions

survival, communications, quick decision making

fight, flight, and freeze

depends on the situation and previous experience with similar situations

environment, sensitization, trauma, and genetic factors (MAC gene plays a role in how we express aggression)

testosterone peaks

aggression and assertive behaviors

low serotonin and cortisol plateus

increase aggressive response

startle reflex

innate, measure of anxiety

heightened in anxious people (tell us if treatment is working)

bed nucleus of the stria terminals and anxiety

where the generalization of fears happens

different neural pathways for…

different fears

cliver-busy damage

damage to both sides of the amygdala

monkeys- increased dangerous actions and decreased fear

humans- unable to experience emotions but can recognize them in others.

anxiety disorders

panic disorder, PTSD (for this class)

PTSD signs

Traumatic event

Re-experienced, increase startle reflex

Avoiding things to do with it

UNable to functions

Month + to diagnose

Arousal increased

Smaller hippocampus increases chances

Benzodiazepines

most common anti-anx med.

GABA (-) agonist- increases inhibition

fascilitates GABA binding to other receptors

inhibition in the amygdala, hypothalamus, midbrain (reticular formation)

muscles relax

alcohol and anxiety

increases GABA, but increases anx in the longrun

decreases glutamate and increases dopamine in the nucleus accumbents (reward circuit)

is stress an emotion?

NO

stress

a non-specific response of the body to demands upon it.

behavioral medicine

branch of med interested in how stress effects health

what systems does stress activate?

sympathetic nervous system- shortterm

HPA Axis- longterm stress

General Adaptation Syndrome

threats to the body activate a general response to stress due to adrenal gland activity.

alarm stage, resistence stage, and exhaustion stages

alarm stage

initial bodily response when confronted with stress, preparing the body to activate

the adrenal glands secrete- epinephrine (+symp. activity), cortisol (+energy), and aldosterone (+blood volume).

resistance stage

decreasing activity to save energy and survive longer.

sympathetic response decreases (less epinephrine from adrenal gland), but cortisol is still released for alertness

exhaustion stage

all energy has been used and the sympathetic NS gives up after prolonged stress. this can lead to breakdowns/burnout and cause stress related illness

this is when the HPA kicks in

stress related illnesses

hypertension, digestive ulcers, high cholesterol, etc.

Hypothalamus Pituitary Adrenal Axis

hypothalamus releases chemicals and activates → pituitary which releases hormone ATCH though the blood to activate→ the adrenal gland which releases cortisol.

cortisol roles

enhanced alertness, increased metabolism, elevates bloodsugar

psychoimmunotherapy

new field studying stress and the immune system response

brief stress on the immune system

good for the immune system, combats infections

but releases prostaglandins (inflammatory) that damage the hypothalamus

prolonged stress on the immune system

depression

poor immunity

memory impairment- cortisol damages the hippocampus

resilliance

how able to cope you are; dependent on genetics, past experience, social support, personality traits (optimism)

how to improve resilliance

exercise, meditation, breathing routines, addressing issues, and distraction,

OPTIMISM

watching caffiene intake, sleeping enough

classical conditioning

pavlov, teaching that a bell signals food, enabling salivation at bell sound alone

operant conditioning

skinner, rat pulls lever, gets good or bad response, initiating more/less behavior.

Lashley

theorized learning and memory happen in the cortex

found that all parts of the cortex help us learn (equipotential) ans that the cortex works as a whole (mass action)

studied rats by teaching them then causing ablations to determine if taught concepts staued

engram

Lashley; physical changes in the brain seen when we make new neural connections (learn)

equipotentiality

all parts of the cortex help us learn

mass action

the cortex works as a whole, the more cortex the better

Thompson

theorized the learning process takes place in the cerebellum (sub cortically)

studied conditioned eye blinks in rabbits, then ablated their brains and tested if it disturbed the learned response.

Lateral Interpositus Nucleus

Thompson; central for learning the conditioned eye blink in rabbits

Multiple Memory Systems

sensory organs take in stimulus

we experience them as sensory memory (1 sec)

if we pay attention they become short-term memories

if we rehearse them, they become long-term memories that we have to retrieve.

working memory- the process of thinking through short-term memories, like a grocery list.

working memory; where in the brain?

actively attending to short term memory for a short peopid of time.

PREFRONTAL CORTEX

longterm memory types

explicit- semantic and episodic (declarative/have to think about)

implicit- procedural, priming/perceptual learning, non-associative learning, simple classical conditioning (emotional and skeletal responses)

explicit memories

DECLARATIVE- have to think about

semantic- facts

episodic- autobiographical, events

### medial temporal lobe and the diencephalon

implicit memories

\
NON-DECLARATIVE- do not have to think about, easier to demonstrate

procedural- striatum

priming/perceptual learning- neocortex

non-associative learning- reflex pathways

simple classical conditioning (emotional and skeletal responses)

amnesia

memory loss

anterograde(future consolidation) , damage to the prefrontal cortex and hippocampus

retrograde (past retrieval), damage to the temporal cortex

or global (total)

anterograde amnesia

(future consolidation) , damage to the prefrontal cortex and hippocampus

retrograde amnesia

(past retrieval), damage to the temporal cortex

Korsakoff’s Syndrome

deficincies in Thalamine (vit. b1) from malnutrition or alcohol abuse

treatable but not reversible, cells around the thalamus die bc they cannot metabolize glucose

causes uses global amnesia, confabulation (false memories), confusion, and apathy

Alzheimer’s Disease

better at procedural memory than semantic (can use a spoon but cannot name it)

neocortex damage- not uniform

paralimbic cortex- most damaged

Neurotransmitters affected- ACh, DA, NA, 5HT, and Glutamate

neuritic plaques

Dementia/ Alzheimers- accumulation of Beta-amyloids

degenerative cellular fragments

neurofibrillary tangles

Dementia/ Alzheimers in neocortex and hippocampus

Hippocampus and memory

does not affect working memory

cannot form new mems, especially episodic

loss of old episodic memories

good procedural memory remains

(can use a spoon, cannot remember story about a spoon from past, cannot form new memories about the spoon either)