PSYC 211: sleep

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methods of studying sleep

brain activity, muscle activity, eye activity

how to record brain activity in sleep

use EEG: attach metal electrodes to scalp to record

sleep states as they progress in night

1st: Non-REM: Deep sleep

as you get closer to waking up: more time spent in REM

how to record muscle activtiy & what you’ll see in REM

attach electrodes to chin to record EMG

• in REM— all muscles relax

how to record eye activity during sleep

attach electrodes to chin to record electromyogram (EMG)

deep, slow wave sleep: REM or non-REM? what type of frequency & amplitude? what type of neuronal firing does this reflect? what kind of activity is this called?

non-REM sleep stage: stages 3,4

• low frequency, high amplitude EEG signals

• synchronized AP bursts

beta activity: what state is someone in? what frequency/amplitude/neural activity

typical of aroused state— high frequency, low amplitude waves reflect desynchronous firing

characteristics of REM sleep

paradoxical sleep— active brain but muscle paralysis

, dreaming- desynchronized neural activity & muscle paralysis

lack of sleep effect on body

severe lack causes death— our mind & immune system to deteriorate

correlation btwn amount of sleep & body mass & what this means

inverse correlation: larger animals don’t have to sleep for very long bc they use energy more efficiently than smaller animals— need less restoration & restoration takes less time for them

waste removal theory

concentration of cellular waste increases in brain across periods of wakefulness & decreases during sleep → sleep is required for efficient waste removal

glymphatic system

helps clear brain’s waste while you’re sleeping, adjacent to lymphatic but for cerebrospinal fluid

ionic gradient rebalancing hypothesis

refutes waste removal theory, we sleep to rebalance ionic gradients to ensure optimal conditions for brain functions (allow ion pumps a break)

brain plasticity/learning & memory/synaptic homeostasis hypothesis

sleep helps reorganize neural network, allows brain time to update itself & synapses, helps w/ memory consolidation

circadian rhythms

controlled by internal biological clock that CONTINUES to run in absence of light, follows 24 hour cycle of behavioral & physiological changes

suprachiasmatic nucelus (SCN) function & whats there

circadian clock is located here, where period genes function

• gets direct input form retinal ganglion cells

period genes

every cell keeps own clock, synapse on each other to create master clock & send out to rest of body (autonomous for each cell but becomes synchronized)

advanced sleep phase syndrome

circadian clock advanced by 4 hrs, mutation in period2 gene

delayed sleep phase syndrome

per3 gene mutation, 4 hour delay in circadian clock

ventrolateral preoptic area (vlPOA) function: what happens if u stimulate vs lesion

key sleep promoting region

electrically stimulate: causes drowsiness & sometimes immediate sleep

lesion: insomnia

sleep/wake flip-flop circuit explained w/ vlPOA & what is means

vlPOA neurons inhibit wake-promoting neurons throughout brain

• vlPOA receives inhibitory inputs from same regions it inhibits (reciprocal inhibiting)

• both regions can’t be actie at same time

adenosine

sleep-promoting molecule, gets stacked up when you’re awake & stimulate vlPOA neurons & inhibits arousing neurons

• gets flushed away during sleep

wake promoting molecules

dop, ser, nor, acetlycholine, histamine

histamine

promotes wakefulness, 1st gen antihistamines promote drowsiness, cross blood-brain barrier

orexin

promotes wakefulness

narcolepsy: what happens & other symptoms

person’s immune system attacks orexins → death of orexin neurons in lateral hypothalamus

other symptoms: sleep-paralysis, cataplexy

sleep paralysis

when REM-associated paralysis occurs just before person falls asleep or right when they wake up

• vivid, dream-like hallucinations

cataplexy

when person experiences complete muscle paralysis while awake— triggered by strong emotional reaction/sudden physical effort (anger, laughter, excitability)

absence of orexin’s general characteristics

blend between “awake” & “asleep” blur

insomnia

can lead to progressive neurodegeneration if symptoms keep worsening— can’t fall asleep/wake up in night

non-rem parasomnias & examples

occur during non-REM sleep or transitions out of sleep

• sleeo walking, talking, groaning (occurs in first half of night, kids grow out of it)

• sleep terrors— can persist w/ PTSD

REM sleep behavior disorder

person doesn’t become paralyzed during REM sleep & acts out their dreams, occurs prior to parkinson’s