Journal
JOURNAL OF NEUROCHEMISTRY
Volume 105, Issue 4, Pages 1480-1498Publisher
WILEY
DOI: 10.1111/j.1471-4159.2008.05257.x
Keywords
adenosine; cytokines; GeneChip (R); neural-immune; quantitative PCR; TaqMan (R) analysis
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Funding
- NHLBI NIH HHS [R01 HL/MH59658, R01 HL059658, R01 HL059658-09, R01 HL059658-07, R01 HL059658-06, R01 HL059658-05, R01 HL059658-08] Funding Source: Medline
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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((R)), 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.
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