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Gene expression in the rat brain during prostaglandin D 2 and adenosinergically‐induced sleep
Author(s) -
Terao Akira,
Huang ZhiLi,
Wisor Jonathan P.,
Mochizuki Takatoshi,
Gerashchenko Dmitry,
Urade Yoshihiro,
Kilduff T. S.
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05257.x
Subject(s) - basal forebrain , sleep (system call) , sleep deprivation , gene expression , forebrain , endocrinology , medicine , hypothalamus , wakefulness , immediate early gene , biology , neuroscience , gene , circadian rhythm , central nervous system , genetics , electroencephalography , computer science , operating system
Previous studies have supported the hypothesis that macromolecular synthesis occurs in the brain during sleep as a response to prior waking activities and that prostaglandin D 2 (PGD 2 ) is an endogenous sleep substance whose effects are dependent on adenosine A 2a receptor‐mediated signaling. We compared gene expression in the cerebral cortex, basal forebrain, and hypothalamus during PGD 2 ‐induced and adenosinergically‐induced sleep to results from our previously published study of recovery sleep (RS) after sleep deprivation (SD). Immediate early gene expression in the cortex during sleep induced by PGD 2 ‐ or by the selective adenosine A 2a agonist CGS21680 showed limited similarity to that observed during RS while, in the basal forebrain and hypothalamus, widespread activation of immediate early genes not seen during RS occurred. In all three brain regions, PGD 2 and CGS21680 reduced the expression of arc , a transcript whose expression is elevated during SD. Using GeneChips ® , the majority of genes induced by either PGD 2 or CGS21680 were induced by both, suggesting activation of the same pathways. However, gene expression induced in the brain after PGD 2 or CGS21680 treatment was distinct from that described during RS after SD and apparently involves glial cell gene activation and signaling pathways in neural‐immune interactions.