Test Bank For Biological Psychology, 14th Edition, James W. Kalat || Complete Guide A+||Latest Update 2024
Test Bank For Biological Psychology, 14th Edition, James W. Kalat Fully Covered Complete Guide A+ Solution ISBN:9781305105409 Newest Version
Test Bank For Biological Psychology, 14th Edition, James W. Kalat || Complete Guide A+||Latest Update 2024
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Rijksuniversiteit Groningen (RuG)
Bachelor Psychology
Biopsychology (PSBA111)
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H8 Wakefulness and Sleep
8.1 Rhythms of Waking and Sleeping
Readiness for season comes partly form internal mechanisms.
Endogenous circannual rhythm = rhythm that prepares for season.
Endogenous circadian rhythm = lasts day. Afect waking, eatng, hormone secton. ight critcal for
resetting circadian rhythms.
Zeitgeber = stmulus that resets circadian rhythm.
People in larger cites less consistent sleeping trend (spend more tme indoor).
Drift out of phase w/ clock insomnia, sleepiness during day. s0% bllind people frequent sleep
probllems.
Jet lag = disrupton of circadian rhythms due crossing tme zones. Mismatch internal & external tme.
Going west phase delay.
Going east phase advance.
Stressful elevated cortsol levels → damage neurons in hippocampus (memory).
Morning of evening person dep on age, genetcs, etc.
Brain generates own rhythms bliological clock. Insensitve to most forms of interference. Main drives
sleep & temp rhythm suprachiasmatic nucleus (SCN), part of hypothalamus.
Interactons among cells sharpen accuracy rhythm. Rhythm followed donors, not recipients
(transplant SCN).
Retnohypothalaicc path from retna to SCN, alter SCN’s setting. Not from normal retnal receptors.
Melanopsin = retnal ganglion cells. Respond mainly to S-wavelength light. Send input to posterior
thalamus. Exposure to S-wavelength light resets circadian rhythm, phase delay.
Genes responsiblle for circadian rhythms period & tmeless promote sleep & inact. Process takes
tme. As concentraton incr, inhiblit mRNA.
ight actvates chemical that blreaks down TIM → incr wakefulness & synchronizing internal clock to
external world.
Mutatons PER lead to altered sleep schedules. Chance of depression.
8.2 Stages of Sleep and Brain Mechanisms
Coma = extended period of unconsc. ow level blrain act & litle/no response to stmuli.
Vegetative state = alternate bletween periods of sleep & moderate arousal, blut no awareness of
surroundings & no purposeful bleh.
Minimally consc state = occasional, blrief periods of purposeful actons & limited amount of speech
comprehension.
Brain death = no sign of blrain actvity & no response to stmulus.
Polysomnograph combli EEG & eye-movement record. Alpha waves = relaxaton. 8-12 Hz.
Sleep spindle = 12-14 Hz. In stage 2. Also K-complex = sharp wave w/ temporary inhibliton of neural
firing.
Stage 3/4 slow-wave sleep (SWS) neural act highly synchronized.
Paradoxical sleep = blrain act relatvely high blut muscles relaxed. Same as rapid eye movement
(REM) sleep. ow-voltage fast waves (incr neural act).
Other stages non-REM (NREM) sleep.
, Amount of REM dep on tme of day rather than how long asleep. REM isn’t dreaming. Dreams more
likely in REM.
Midblrain own mechanism to promote wakefulness. Decr arousal bly damaging reticular formation.
Some axons ascending to blrain & spinal cord (motor control).
Retcular formaton part that contriblutes to cortcal arousal = Pontomesencephalon. Receive input
from many sensory syst & generate spontaneous act. Axons extend to foreblrain, release
acetylcholine, glutamate → excite cells (hypo)thalamus & basal forebrain. Stmulaton awakens
sleeping ind or incr alertness.
Locus coeruleus = small structure in pons. Usually inact, blut blursts of impulses to meaningful events
(emotonal arousal). Output incr act most act neurons & decr act least actve neurons. Enhanced
atenton & memory.
Inf arousal hcstaicne enhances arousal & alertness.
Pathway from hypothalamus released orexin/hypocretin. Enhance wakefulness. Staying awake.
Block orexin receptors help go to sleep.
Pathway lateral hypothalamus regulates cells blasal foreblrain. Release acetylcholine (incr arousal).
Sleep dep on decr sensory input in cereblral cortex. Cells thalamus hyperpolarized. Moderate sensory
input remains.
Unconsc due inhibliton (GABA). Sleep can ble local in blrain, sublstantal inhibliton in 1 area & not in
another blv sleepwalking & lucid dreaming (bleing aware of dreaming).
Pons & medulla inhiblit spinal neurons that control muscles during REM. Damage actng out dreams.
REM incr act in pons, limblic syst, parietal & temporal cortex. Decr in V1 motor cortex, dorsolateral
PFC.
PGO waves = high-amplitude electrical potentals.
Waves of neural act pons → lateral geniculate nucleus → occipital cortex.
REM dep on serotonin & acetylcholine.
Insomnia dep on how person feels following day. Many dif causes. Circadian rhythms. Phase
delayed troublle falling asleep. Phase advanced wakens early.
Sleep apnea = impaired ablility to blreathe while sleeping. Interruptng sleep bly waking up.
Areas blrain lost neurons deficiencies learning, reasoning, atenton, impulse control.
Sleep impairments responsiblle for cogn loss.
Causes genetc, hormones, old-age deterioraton blrain mechanisms regulatng blreathing,
oblesity.
Narcolepsy = frequent periods of sleepiness during day.
Symptoms sleep atacks, cataplexy (atack of muscle weakness), sleep paralysis, hypnagogic
hallucinatons.
Cause lack hypothalamic cells that produce orexin.
Periodic limb movement disorder = repeated involuntary movement during sleep. Mostly
during NREM sleep.
REM beh disorder = move around during REM, actng out dreams. Deficient GABA.
Night terrors = intense anxiety from which person awakens screaming in terror. More severe than
nightmares.
Sleepwalking deeds poorly planned, blecause blrain areas inact. ike sexsomnia engage in sexual bleh
while sleeping.
8.3 Why Sleep? Why REM? Why Dreams?
During sleep rest muscles, decr metablolism, perform cellular maintenance in neurons, reorganize
synapses, strengthen memories.
Sleep deprivaton act immune syst, mental illness, save energy during inefcient tmes.
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