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Caffeine treatment prevents rapid eye movement sleep deprivation‐induced impairment of late‐phase long‐term potentiation in the dentate gyrus
Author(s) -
Alhaider Ibrahim A.,
Alkadhi Karim A.
Publication year - 2015
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13092
Subject(s) - creb , dentate gyrus , long term potentiation , hippocampus , caffeine , sleep deprivation , endocrinology , medicine , brain derived neurotrophic factor , rapid eye movement sleep , neuroscience , chemistry , psychology , neurotrophic factors , circadian rhythm , receptor , biochemistry , electroencephalography , transcription factor , gene
The CA 1 and dentate gyrus ( DG ) are physically and functionally closely related areas of the hippocampus, but they differ in various respects, including their reactions to different insults. The purpose of this study was to determine the protective effects of chronic caffeine treatment on late‐phase long‐term potentiation (L‐ LTP ) and its signalling cascade in the DG area of the hippocampus of rapid eye movement sleep‐deprived rats. Rats were chronically treated with caffeine (300 mg/L drinking water) for 4 weeks, after which they were sleep‐deprived for 24 h. L‐ LTP was induced in in anaesthetized rats, and extracellular field potentials from the DG area were recorded in vivo . The levels of L‐ LTP ‐related signalling proteins were assessed by western blot analysis. Sleep deprivation markedly reduced L‐ LTP magnitude, and basal levels of total cAMP response element‐binding protein ( CREB ), phosphorylated CREB (P‐ CREB ), and calcium/calmodulin kinase IV (Ca MKIV ). Chronic caffeine treatment prevented the reductions in the basal levels of P‐ CREB , total CREB and Ca MKIV in sleep‐deprived rats. Furthermore, caffeine prevented post‐L‐ LTP sleep deprivation‐induced downregulation of P‐ CREB and brain‐derived neurotrophic factor in the DG . The current findings show that caffeine treatment prevents acute sleep deprivation‐induced deficits in brain function.