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