Benington J H, Woudenberg M C, Heller H C
Department of Biological Sciences, Stanford University, CA 94305, USA.
Brain Res. 1995 Sep 18;692(1-2):86-92. doi: 10.1016/0006-8993(95)00591-d.
To determine the role of neuronal potassium conductance in rapid-eye-movement (REM)-sleep homeostasis, we have administered small doses of apamin (2-5 ng), a selective blocker of the calcium-dependent SK potassium channel, injected into the lateral ventricle in rats, and characterized the resultant effects on REM-sleep expression. Apamin produces a dose-dependent reduction in REM-sleep expression without an increase in the frequency of attempts to enter REM sleep, suggesting that accumulation of REM-sleep propensity is suppressed. The vast majority (84-95%) of lost REM sleep is not recovered 40 h after apamin administration. These findings suggest that accumulation of REM-sleep propensity is linked to the increased neuronal potassium conductance in nonREM sleep.
为了确定神经元钾电导在快速眼动（REM）睡眠稳态中的作用，我们向大鼠侧脑室内注射了小剂量（2 - 5纳克）的蜂毒明肽（一种钙依赖性SK钾通道的选择性阻滞剂），并对由此产生的对REM睡眠表现的影响进行了表征。蜂毒明肽使REM睡眠表现呈剂量依赖性降低，而进入REM睡眠的尝试频率并未增加，这表明REM睡眠倾向的积累受到了抑制。在注射蜂毒明肽40小时后，绝大多数（84 - 95%）失去的REM睡眠并未恢复。这些发现表明，REM睡眠倾向的积累与非快速眼动睡眠中神经元钾电导的增加有关。
