Lecture 11 flip flop Flashcards
What are the brain regions that promote wakefulness
wakefulness - cell groups projecting to the thalamus, hypothalamus, basal orebrain, cortex
orexin/hypocretin - lateral hypothalamus, excitatory influence, controller of wakefulness
What are some examples of using drugs to promote/decrease wakefulness?
What is the underlying mechanism?
amphetamine - NA agonist
AMPT - NA antagonist
NA cells concentrated in LC, project to all areas of the brain, particularly the thalamus and hypothalamic structures
LC more active during wakefulness than sleep
What areas of the brain is active/not active during wake/NREM sleep
Preoptic area super active during sleep
TMN, BF and LC more active during awake
Describe the orexin/hypocretin mechanism
cell bodies located in lateral hypothalamus
hypocretin/orexin - neurotransmitter
neurons active during wake
excitatory projections to TMN, Raphe, LC, PPT, LDT, BF, cortex - therefore synchronized functions
What is VLPO
ventrolateral pre-optic nucleus - anterior hypothalamus - inhibit wakefulness and being inhibited by wakefulness (including orexine neurons)
GABA and galanin, inhibitory
How does VLPO influence sleep and be influenced by sleep
Elevated activity during sleep, but not deprivation
lesion
core VLPO - NREM loss
extended VLPO - REM loss
however, full lesion only results in 50% sleep loss - another mechanism must exist
What is the role of Basal forebrain (with evidence)
stimulating BF causes cats to be drowsy
lesions of VLPO and basal forebrain however results in temporary sleep loss - sleep miraculously return to baseline after a few weeks (systems able to compensate for each other)
Why is the system so stable given so many inputs?
flip-flop switch
Describe the flip-flop switch for sleep and wake and how the switch is triggered
sleep side - VLPO + VLPO ex = sleep
promoted by homeostatic sleep drive + circadian hypnotic signal, inhibit orexin
inhibit TMN and LC Raphe
wake side - TMN LC - Raphe = wake
promoted by circadian alerting signal + orexin
inhibit VLPO
Rem sleep-on neurons
- GABA neurons in SLD - active in REM, inhibit REM off
- cholinergic cells in LDT/PPT - swtich for REM on
3.LDT/PPT active during REM, moderately active during wakefulness, inactive during NREM
(activation of LDT/PPT may be the reason why eeg for REM and wakefulness looks similar??)
- LDT/PPT stimulate other pontine structure for REM (what does that mean, go back to lectures)
REM-off neurons
vlPAG/LPT - GABA neuron inhibiting REM
inactive during REM and active during NREM and waking - inhibit SLD and REM sleep
activated by LC and raphe
inhibited by ex VLPO
the role of orexin in REM
orexin stimulates arousal - inhibites VLPO
stimulates LC and Raphe - inhibites REM
low level of orexin = likelihood of REM (but something needs to start REM)
thus low level of orexin during wakefulness = difficulty maintaining wafefulness and possibility of REM intrusion
Describe the flip-flop switch for NREM and REM
REM on side - SLD receiving excitatory input from PPT/LDT
inhibiting vlPAG, IPT, LE, Raphe
REM off side - vlPAG, LPT receiving excitatory input from LC Raphe, orexin
inhibited by exVLPO, LDT, SLD
inhibiting SLD
Difference of activity level - LDT/PPT, LC/TMN
VLPO, VLPO ex, orexin
I cannot be bothered bit check the sleep stages and physiological activity for detail
LDP/PPT moderately active during wakefulness, very active during REM
LC/DR/TMN - very active during wakefulness, active during NREM
VLPO - very active during NREM, active during REM
VLPO ex - active durign NREM, very active during REM
orexin - active during wakefulness
NANI THE FUCK is this lecture about????
Sleep and wakefulness are each initiated by a number of different brain structures.
These are coordinated by the orexin system during wakefulness and VLPO during NREM sleep.
Stable sleep and wakefulness are achieved by reciprocal inhibition of the two systems, what has been referred to as the flip-flop switch.
The monoamines and acetylcholine interact in a similar manner to control REM sleep.
