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Activation of c‐ fos in GABAergic neurones in the preoptic area during sleep and in response to sleep deprivation
Author(s) -
Gong Hui,
McGinty Dennis,
GuzmanMarin Ruben,
Chew KengTee,
Stewart Darya,
Szymusiak Ronald
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.056622
Subject(s) - gabaergic , sleep (system call) , endocrinology , medicine , sleep deprivation , glutamate decarboxylase , c fos , circadian rhythm , neuroscience , chemistry , biology , inhibitory postsynaptic potential , gene expression , biochemistry , computer science , gene , enzyme , operating system
Neurones in the median preoptic nucleus (MnPN) and the ventrolateral preoptic area (vlPOA) express immunoreactivity for c‐Fos protein following sustained sleep, and display elevated discharge rates during both non‐REM and REM sleep compared to waking. We evaluated the hypothesis that MnPN and vlPOA sleep‐active neurones are GABAergic by combining staining for c‐Fos protein with staining for glutamic acid decarboxylase (GAD). In a group of six rats exhibiting spontaneous total sleep times averaging 82.2 ± 5.1% of the 2 h immediately prior to death, >75% of MnPN neurones that were Fos‐immunoreactive (IR) were also GAD‐IR. Similar results were obtained in the vlPOA. In a group of 11 rats exhibiting spontaneous sleep times ranging from 20 to 92%, the number of Fos + GAD‐IR neurones in MnPN and vlPOA was positively correlated with total sleep time. Compared to control animals, Fos + GAD‐IR cell counts in the MnPN were significantly elevated in rats that were sleep deprived for 24 h and permitted 2 h of recovery sleep. These findings demonstrate that a majority of MnPN and vlPOA neurones that express Fos‐IR during sustained spontaneous sleep are GABAergic. They also demonstrate that sleep deprivation is associated with increased activation of GABAergic neurones in the MnPN and vlPOA.