Basheer Radhika, Bauer Andreas, Elmenhorst David, Ramesh Vijay, McCarley Robert W
Laboratory of Neuroscience, Boston VA Healthcare System-Harvard Medical School, West Roxbury, Massachusetts 02132, USA.
Neuroreport. 2007 Dec 3;18(18):1895-9. doi: 10.1097/WNR.0b013e3282f262f6.
Sleep deprivation increases the levels of extracellular adenosine and A1 receptor (A1R)mRNA in the cholinergic zone of the basal forebrain, a region involved in sleep homeostasis. To evaluate homeostatic control mechanisms, we examined the sleep deprivation-induced changes in the A1R density in rodent brain using [H]CPFPX receptor autoradiography. We also examined the role of nuclear factor-kappaB (NF-kappaB) in transcriptional upregulation of A1R mRNA by use of the inhibitor peptide SN50 to inhibit nuclear translocation of NF-kappaB. We found a significant increase in cholinergic basal forebrain A1R density following 24 h of sleep deprivation and evidence that the upregulation of A1R is mediated by NF-kappaB. The A1R increase may be important in sleep homeostasis, since the increase in A1R density would increase the inhibitory effect of given level of adenosine, thus increasing the gain of the homeostat.
睡眠剥夺会增加基底前脑胆碱能区细胞外腺苷和A1受体（A1R）mRNA的水平，该区域参与睡眠稳态。为了评估稳态控制机制，我们使用[H]CPFPX受体放射自显影技术检测了睡眠剥夺诱导的啮齿动物脑内A1R密度变化。我们还通过使用抑制剂肽SN50抑制核因子-κB（NF-κB）的核转位，研究了NF-κB在A1R mRNA转录上调中的作用。我们发现睡眠剥夺24小时后胆碱能基底前脑A1R密度显著增加，并且有证据表明A1R的上调是由NF-κB介导的。A1R的增加可能在睡眠稳态中很重要，因为A1R密度的增加会增强给定水平腺苷的抑制作用，从而增加稳态调节器的增益。
