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Adenosine and sleep deprivation promote NF‐κB nuclear translocation in cholinergic basal forebrain

In our investigations related to the homeostatic sleep factor adenosine (AD), we previously demonstrated that the DNA‐binding activity of the transcription factor NF‐κB in rat cholinergic basal forebrain increased following 3 h of sleep deprivation (SD). However, the neurotransmitter nature of the cells and the SD‐induced stimuli responsible for NF‐κB activation were not defined. In this report, we demonstrate, using double labeling immunohistochemistry, that nuclear translocation of NF‐κB occurs almost exclusively in the cholinergic neurons of the basal forebrain following 3 h of SD. Furthermore, cholinergic basal forebrain microinjection of AD (25 nmol/L) or the A1 receptor agonist N6‐cyclo‐hexyladenosine (100 nmol/L) induced nuclear translocation of NF‐κB, thus suggesting that SD‐induced increased extracellular concentrations of AD, acting via the A1 AD receptor, may be responsible for the nuclear translocation of NF‐κB in cholinergic neurons. Moreover, blocking the nuclear translocation of NF‐κB by injection of inhibitor peptide, SN50, immediately prior to 6 h SD significantly reduced delta activity (1–4 Hz) during the first two hours of recovery sleep. Together, these data suggest a role in sleep homeostasis for the SD‐induced activation of NF‐κB in cholinergic basal forebrain, and that transcription factor NF‐κB may code for factor(s) that play a role in sleep homeostasis.