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9 Neural mechanisms of sleep (Histamines # (Antihistamines (First…
9 Neural mechanisms of sleep
Brain areas
Reticular formation
generates wakefullness
Thalamus
damage severely impairs consciousness but sleep cycle stays intact
2 types of neurons
glutamate
gaba
Pons
important for generation of REM
SCN
Master pacemaker
regulates circadian rhythms
uses light-dark
2 pathways of arousal system
important?
cholinergic neurons innervate thalamus nuclei
monoaminergic neurons
LC.......
both activate cerebral cortex
Preoptic area
Median
activate with sleep deprivation
respond to buildup of adenosine
activate ventrolateral preoptic neurons
fire during sleep
ventrolateral
active when asleep
GABA
ARAS
Waking system
ascending arousal system
2 pahtways
Dorsal
to thalamus, information to cortex
ACh ppt, ldt
Reticular nucleus
gating between thalamus and cortex
Ventral
via hypothalamus?
Serotonergic nuclei: dorsal raphe nucleus and median raphe nucleus
Dopaminergic nuclei: ventral tegmental area and substantia nigra pars compacta
Noradrenergic nuclei: locus coeruleus and related brainstem nuclei
Histaminergic nuclei: tuberomamillary nucleus
Cholinergic nuclei: forebrain cholinergic nuclei and cholinergic nuclei in the pontine tegmentum (laterodorsal tegmental nucleus and pedunculopontine nucleus)
Thalamic nuclei: thalamic reticular nucleus and intralaminar nucleus, particularly the centromedian nucleus
Sleep switch
Wake
high monoamine and choline
inhibit VLPO
disinhibition of arousal regions
Sleep
Preoptic neurons active
inhibit arousal regions
disinhibit own firing?
Mutual inhibition
produces stable states
only 2% of the time is in transition
Orexin
#
stabelizes states
reinforces mutual inhibition
REM-NREM
REM
SLD
NREM
VLDG
Histamines
#
Promote wakefulness
Posterior hypothalamus
tuberomamillary nucleus
activity
highest in wakefullness, lowest in REM
Reduced in nacolepsy and hypersomnia
#
maintaining arousal
Antihistamines
First generation
H1-receptor antagonists
Occupies receptor and block histamine
frontal lobe and deep structures
Lipohpilic
cross blood-brainbarrier
sedation
perfomance deficits
divided attention, working memory, vigilance and speed
But often not perceived
Second generation
Difficult through blood brain barrier
Different ionic charge
larger molecules
More lipophobic
only occupy 20% of receptors
circadian rhythmicity
Excited by dopamine and Orexine
Narcolepsy
Loss of orexin
problems maintaining state
Flip flop switch does not work properly
symptoms
Difficulty maintaining wake or sleep
Cataplexy
lose of muscle tone after strong emotion
REM atonia
Sleep paralyses
Weight gain
less apetite but even less exercise
circadian rhythm stabilizes metabolism so metabolism is off
Relation between food and sleep but not well understood
Neurochemical systems
Acetylcholine (ACh)
For Wakefulness and REM
brainstem, basal forebrain, pons
Norepinephrine (NE)
generate arousal during high attention
important/stressful stimuli
LC
most active during wakefullnes, silent in REM
Serotonin
promotes wakefulness and suppresses REM
Raphe nucleus
Dopamine
wake promoting
high in waking low in NREM
Promote arousal in motivation and physical activity
Substantia nigra, VTA, PAG
Orexin
Fire during wakefulness and silent in sleep
activated by movement (walking)
increase arousal with activity and suppress sleep
Lost in narcolepsy
#
Sustaining wakefulness and sleep?
Stabilizes flipflop
exites neurons that inhibit REM
Posterior lateral hypothalamus
Exitatory
hypothalamus
Adenosine
Promotes sleep
when high energy
levels are low
when low energy
Less ATP production
Adenosine goes up
acts as inhibitory substance
promotes sleep
Early research
von Economo
described Encephalitis Lethargica
One group became excessively sleepy
abnormal eye movement
Lesions in caudal 3th ventricle and cerebral aqueduct
other group had insomnia
movement disorders
lesions in rostral 3th ventricle and basal ganglia
survivors may develop narcolepsy
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