Benington J H, Kodali S K, Heller H C
Department of Biological Sciences, Stanford University, CA 94305, USA.
Brain Res. 1995 Sep 18;692(1-2):79-85. doi: 10.1016/0006-8993(95)00590-m.
N6-Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, increased EEG slow-wave activity in nonREM sleep when administered either systemically (0.1-3 mg/kg) or intracerebroventricularly (3.5-10 micrograms) in the rat. The power spectrum of EEG changes (as calculated by Fourier analysis) matched that produced by total sleep deprivation in the rat. The effects of CPA on the nonREM-sleep EEG were dose-dependent. These findings suggest that adenosine is an endogenous mediator of sleep-deprivation induced increases in EEG slow-wave activity, and therefore that increased adenosine release is a concomitant of accumulation of sleep need and may be involved in homeostatic feedback control of sleep expression.
N6-环戊基腺苷（CPA），一种A1腺苷受体激动剂，当以全身给药（0.1 - 3毫克/千克）或脑室内给药（3.5 - 10微克）方式给予大鼠时，会增加非快速眼动睡眠期的脑电图慢波活动。脑电图变化的功率谱（通过傅里叶分析计算）与大鼠完全睡眠剥夺所产生的功率谱相匹配。CPA对非快速眼动睡眠脑电图的影响具有剂量依赖性。这些发现表明，腺苷是睡眠剥夺诱导的脑电图慢波活动增加的内源性介质，因此腺苷释放增加是睡眠需求积累的伴随现象，并且可能参与睡眠表达的稳态反馈控制。
