TY  - CHAP
M1  - Book, Section
TI  - Sleep and Arousal
A1  - Nestler, Eric J.
A1  - Kenny, Paul J.
A1  - Russo, Scott J.
A1  - Schaefer, Anne
PY  - 2020
T2  - Nestler, Hyman & Malenka’s Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 4e
AB  - KEY  CONCEPTSStates  of  sleep  and  wakefulness  are  both  active  processes  mediated  by  specific  brain  regions  and  neurotransmitter  systems.Drowsiness  is  a  state  of  diminished  vigilance  that  occurs  in  transitions  between  wake  and  sleep.  Sleep  itself  can  be  divided  into  two  phases,  nonrapid  eye  movement  (nonREM)  and  REM  sleep,  the  latter  being  characterized  by  brain  activity  resembling  that  observed  during  the  waking  state.The  physiologic  functions  of  distinct  phases  of  sleep  are  unknown.  Overall,  the  timing  and  quality  of  sleep  may  play  important  roles  in  memory  consolidation  and  metabolic  processes.The  initiation  of  nonREM  sleep  is  controlled  in  part  by  GABAergic  neurons  in  the  preoptic/anterior  hypothalamic  area;  the  initiation  of  REM  sleep  is  controlled  by  cholinergic  cells  in  the  pontine  tegmentum  in  the  brainstem.  Many  additional  nuclei  contribute  to  the  regulation  of  sleep  and  wake  time.Sleep  is  controlled  both  by  circadian  rhythms  and  by  the  homeostatic  drive  produced  by  periods  of  wakefulness.  Adenosine  is  an  important  mediator  of  the  homeostatic  drive  for  sleep.The  suprachiasmatic  nucleus  is  the  primary  pacemaker  for  the  circadian  regulation  of  sleep  and  other  physiologic  processes,  in  particular,  for  entraining  circadian  rhythms  to  environmental  light.Circadian  rhythms  are  produced,  in  part,  by  the  complex  transcriptional  regulation  of  “clock”  genes  that  have  been  conserved  throughout  evolution.Sleep  disorders  are  a  significant  cause  of  morbidity  and  mortality.Narcolepsy  is  a  sleep  disorder  characterized  by  abnormal  regulation  of  sleep–wake  cycles.  Most  cases  are  caused  by  the  autoimmune  destruction  of  the  brain’s  orexin–containing  neurons  in  the  lateral  hypothalamus.Benzodiazepines  and  similarly  acting  drugs,  which  are  positive  allosteric  modulators  of  GABAA  receptors,  are  the  most  common  pharmacologic  treatments  for  insomnia.  Orexin  receptor  antagonists  are  a  more  recently  introduced  class  of  anti-insomnia  medications.General  anesthetics,  comprising  diverse  classes  of  compounds,  induce  a  transient  coma  that  resembles  nonREM  sleep  electrophysiologically,  and  is  clinically  characterized  by  global  amnesia,  analgesia,  and  nonresponsiveness.  Most  general  anesthetics  act,  at  least  in  part,  by  facilitating  inhibitory  ion  channels  (including  ligand–gated  channels)  or  inhibiting  excitatory  ion  channels.  
SN  - 
PB  - McGraw-Hill
CY  - New York, NY
Y2  - 2024/04/19
UR  - neurology.mhmedical.com/content.aspx?aid=1174974413
ER  -