Sleep

Sleep Disorders

Reasons for Sleeping

Sleep Physiology

Neuroscience of Sleep

recovery from wakeful mental activity

growth hormone

immune activity

replenish brain glycogen

consolidate memories

synaptic homeostasis hypothesis

signal to noise ratio

want high signal to noise ratio – easier to hear signal when noise is low

as go through day becomes harder to separate signal from noise

sleep helps improve signal to noise ratio

brain eliminates new synapses that are just noise

preserves synapses that are important information

negative effects of sleep deprivation = evidence for homeostatic drive for sleep

fatal familial insomnia

cognitive impairment

REM reboudn

Insomnia

Paradoxical Insomnia

Sleep apnea

Narcolepsy

REM sleep behavior disorder

genetic defect in orexin activity

treatment: medication – provigil

failed motor inhibition

prognosis: progressive, neurodegenerative

respiratory obstruction

treatment: continuous positive airway pressure (CPAP)

hyperarousal during sleep time

treatment: address stressor

sleep state msiperception

treatment: reassurance that patient is actually sleeping

wakefulness

active & deliberate sensorimotor engagement w/ environment

awareness & memory formation

sleep

loss of consciousness

lack of memory formation

not lack of mental activity

studied by sleep labs – diagnose sleep disorders

Electroencephalogram (EEG)

measures summation of activity of thousands of neurons

recording neural aggregates

irregular

synchronized

neural activity similar among neurons (spikes occurs @ same time in each neuron)

EEG sum = low frequency activity, high amplitude

unrelated neural activity among many neurons

EEG sum = high frequency activity, low amplitude

showed precise & dramatic changes during sleep

Typical Sleeping EEG

Alpha Rhythms (Awake)

(1) Beta Rhythms (REM)

(2) Theta Rhythms (stage 1 non-REM)

(3) Spindle (stage 2 non-REM)

(4) Delta Rhythms (stage 3&4 non-REM)

relaxed

not thinking of anything in particular

i.e. daydreaming

seen during more concentrated tasks

i.e. math homework, making grocery list

more amplitude & less frequency than alpha & beta

large changes in amplitude (larger change in amplitude = K complex)

even larger changes in amplitude up until stage 4

after stage 4 return to beta rhythms (REM sleep)

closer to morning = longer bouts of REM sleep & vice versa

non-REM & REM alternate in 90 mins cycles

REM = paradoxical, beta-like, desynchronized vs. non-REM = synchronized, slow wave

mental activity

REM – vivid, visual hallucination

non-REM – emotional dreams

sleep science

high spinal transections does not prevent sleep-wake cycles

pons = source of REM sleep & simultaneous motor inhibition

brain has specific, localized mechanism to regulate sleep

lesion to pons would disrupt REM

lesion to its descending neurons would prevent sleep motor inhibition

arousal systems

"reticular activating system"

axons widely branching in the forebrain

histamine – vigilance

acetylcholine – executive function

norepinephrine – set-shifting, attention

serotonin – response inhibition, reversal learning

Orexin/Hypocretin

peptide made in dorsal/lateral hypothalamus

linked to narcolepsy

knock out mice

narcoleptic dogs have mutation in receptor

narcoleptic people suffer from loss of orexin neurons

flip-flop control of sleep vs. wakefulness

sleep center = ventrolateral preoptic area (VLPO) – has ability to inhibit all arousal centers

lesions cause deficit in sleep time

GABA-ergic input to arousal centers, mutual flip-flop circuit (quick switch between states)

sleep onset

VLPO activator = adenosine (metabolite of ATP)

accumulation of adenosine = indicative of neuronal depletion of energy stores

caffeine blocks adenosine receptors

flip-flop control of REM vs. non–REM

REM-on neurons (ACh in pons)

motor inhibition; eye movements; genital blood flow; cortical arousal (dreams)

midbrain: REM-off neurons

mutual inhibition – orexin promotes REM-off

w/ sleep onset, orexin shuts off –> disinhibiting REM-on