Sleep Flashcards
Slow wave sleep
Brain relatively inactive -energy expenditure low
Synchronized slow waves in EEG
Muscles relaxed but body capable of movement
-e.g. postural adjustment
Some dreaming but less vivid
REM sleep
Brain as active as during consciousness -energy expenditure high
Desynchronized EEG -similar to that of consciousness
Body paralyzed to prevent movement
Movements of the eyes
Occurrence of vivid dreams
Blocking the sleep phases
REM and SW sleep can be selectively blocked
If REM sleep prevented there is a rebound in amount of REM sleep
Similarly for SW sleep
There are separate neural control mechanisms for the two phases of sleep, and they may have different functions.
Sleep habits link to common cold
Those volunteers with less than 7 hours sleep/night were nearly 3x more likely to get a cold than those with 8 hours or more
Those volunteers with less than 92% sleep efficiency were 5.5x more likely to get a cold than those with 98% or greater sleep efficiency
Development of REM sleep
Infants born 10 weeks prematurely REM sleep 80% of total sleep
At 2-4 weeks premature this is 60-65%
At normal term REM sleep drops to ~50%
And at age of 2 REM sleep comprises 30-35%
But adults still have REM sleep (~25% of total)
Sleep flushes out brain waste
Extracellular space increases during sleep
Effect of sleep deprivation
no REM = less performance improvement
no SW = improvement
nap also improves
What are place neurons
Neurons in the hippocampus have spatial receptive fields –called “place neurons”
Basal forebrain controls sleep
Basal forebrain consists of several areas close to each other
Substantia innominata
Nucleus of the diagonal band
Medial septum
Magnocellular preoptic nucleus
Loss of neurons in these areas associated with Alzheimer’s disease
Neuron of the basal forebrain –active during SW (NREM) sleep
Neurons of the basal forebrain have state dependent activity
Further evidence linking basal forebrain to SW sleep
Lesions of basal forebrain produce insomnia
Low frequency stimulation of basal forebrain can induce sleep and EEG synchronization
Basal forebrain contains cholinergic neurons that project to cortex and form part of the arousal system
Inhibition of these neurons leads to SW sleep
REM sleep is controled by..
REM on Cholinergic which fire before period of REM sleep
Effector neurons
REM off NA and 5HT start to fire during REM
5-HT, histamine and noradrenaline are monoaminergic transmitters and forms ascending arousal system
Histamine is a NT that helps to induce wakefulness
How is SW and REM sleep organised
Linked and organised in a cyclical fashion
Discovery of orexin/hypocretin (recent development in field)
Discovered simultaneously as a mRNA transcript enriched in hypothalamus, and as a brain-derived peptide that stimulated “orphan” receptors (GPCR with no known agonist) and increased food intake
There are two peptides orexin A (can act at2 receptors) and B (acts on one receptor) produced from a prepro-orexin product and two receptors
Unexpected role for orexin in narcolepsy
Narcolepsy is a disorder of REM sleep where subjects suddenly fall asleep (“sleep attack”), can involve sudden loss of muscle tone (cataplexy)
Knock-out of prepro-orexin gene gives narcoleptic symptoms in mice
Study of narcolepsy in dogs identified a single gene canarc-1 for narcolepsy, this turned out to code for a defective orexin-2 receptor
Human narcoleptics
Genetics of narcolpesy more complex –do not have same mutant receptors as dogs
They lack orexin-positive neurons in the lateral hypothalamus (in situ and immunocytochemistry)
Cannot detect orexins in CSF of these patients
The orexinergic neurons project to many of the nuclei involved in control of sleep
Orexin seems to stabilize wakefulness and prevent rapid switching to sleep and back again
