Serotonin hyperpolarizes cholinergic low-threshold burst neurons in the rat laterodorsal tegmental nucleus in vitro.
Serotonin hyperpolarizes cholinergic low-threshold burst neurons in the rat laterodorsal tegmental nucleus in vitro.
复制标题
体外血清素使大鼠背侧被盖核中的胆碱能低阈值爆发神经元超极化。
DOI：
10.1073/pnas.89.2.743
复制
发表时间：
1992
影响因子：
11.1
通讯作者：
Reiner,PB
中科院分区：
文献类型：
--
作者：
Luebke,JI;Greene,RW;Semba,K;Kamondi,A;McCarley,RW;Reiner,PB
胆碱能神经元活动的5-羟色胺能抑制与快速眼动睡眠的调节及其相关的现象，脑桥枕叶波，一直被假定，但没有直接的证据。本研究采用细胞内和全细胞膜片钳记录技术结合酶组织化学方法，研究了体外培养的大鼠被盖背外侧核胆碱能神经元的内在电生理特性及其对5-羟色胺（5-HT）的反应。65%的记录神经元表现出突出的低阈值爆发，其中83%是胆碱能的。在电流钳记录64%的爆裂胆碱能神经元测试响应的应用程序5-HT与膜超极化和输入电阻下降。通过应用选择性5-HT 1型受体激动剂羧酰胺色胺马来酸盐来模拟这种作用。全细胞膜片钳记录显示，超极化反应是由内向整流钾电流介导的。应用5-HT降低兴奋性和显着调制的胆碱能爆发神经元的放电模式：在5-HT诱导的超极化这些神经元表现出无反弹爆发后，超极化电流输入和爆发响应于去极化电流输入。在5-HT缺乏的情况下，相对去极化的胆碱能爆发神经元响应于相同的超极化电流输入与爆发和去极化电流输入后不产生爆发。这些数据提供了一个细胞和分子基础的假设，5-HT调制快速眼动睡眠现象，通过改变突发胆碱能神经元的放电模式。
Serotonergic suppression of cholinergic neuronal activity implicated in the regulation of rapid eye movement sleep and its associated phenomenon, pontogeniculooccipital waves, has long been postulated, but no direct proof has been available. In this study, intracellular and whole-cell patch-clamp recording techniques were combined with enzyme histochemistry to examine the intrinsic electrophysiological properties and response to serotonin (5-HT) of identified cholinergic rat laterodorsal tegmental nucleus neurons in vitro. Sixty-five percent of the recorded neurons demonstrated a prominent low-threshold burst, and of these, 83% were cholinergic. In current-clamp recordings 64% of the bursting cholinergic neurons tested responded to the application of 5-HT with a membrane hyperpolarization and decrease in input resistance. This effect was mimicked by application of the selective 5-HT type 1 receptor agonist carboxamidotryptamine maleate. Whole-cell patch-clamp recordings revealed that the hyperpolarizing response was mediated by an inwardly rectifying K+ current. Application of 5-HT decreased excitability and markedly modulated the discharge pattern of cholinergic bursting neurons: during a 5-HT-induced hyperpolarization these neurons exhibited no rebound burst after hyperpolarizing current input and a burst in response to depolarizing current input. In the absence of 5-HT, the relatively depolarized cholinergic bursting neurons responded to an identical hyperpolarizing current input with a burst and did not produce a burst after depolarizing current input. These data provide a cellular and molecular basis for the hypothesis that 5-HT modulates rapid eye movement sleep phenomenology by altering the firing pattern of bursting cholinergic neurons.