Imon H, Ito K, Dauphin L, McCarley R W
Department of Psychiatry, Harvard Medical School, Brockton, MA 02401, USA.
Neuroscience. 1996 Sep;74(2):393-401. doi: 10.1016/0306-4522(96)00134-0.
A large and consistent body of data implicates mesopontine cholinergic neurons in the production of rapid eye movement sleep, and indicates that many rapid eye movement sleep events are mediated by activation of pontine reticular formation neurons. There is anatomical evidence for projections from the mesopontine cholinergic nuclei to the pontine reticular formation, but no study has shown that stimulation of this cholinergic zone produces excitatory postsynaptic potentials in pontine reticular formation neurons. In the present study, intracellular recording were made from 168 pontine reticular formation neurons, identified by antidromic activation from the bulbar reticular formation and by neurobiotin intracellular labeling, in acutely anesthetized cats. The effects of single-pulse electrical stimulation of the laterodorsal tegmental nucleus portion of the ipsilateral mesopontine cholinergic zone were evaluated in these neurons. Under urethane anesthesia this stimulation produced, in 21 of 22 recorded neurons, long-latency excitatory postsynaptic potentials (mean = 3 ms), consistent with the conduction velocity of unmyelinated cholinergic fibers (measured conduction velocity was 2 m/s). This excitatory postsynaptic potential was virtually abolished by intravenous administration of the muscarinic cholinergic receptor blocker scopolamine (n = 40 neurons), and by acute cuts separating the laterodorsal tegmental nucleus and the recorded neurons (n = 40). In contrast, a short-latency excitatory postsynaptic potential (0.7-1.5 ms) was not reduced in amplitude by scopolamine and could still be elicited following acute transverse cuts. Unlike the longer-latency excitatory postsynaptic potential, its amplitude was not reduced by barbiturate anesthesia. These data, suggesting the presence of an excitatory, cholinergic laterodorsal tegmental nucleus projection to the pontine reticular formation, provide further support to other lines of evidence implicating mesopontine cholinergic neurons in the production of rapid eye movement sleep, and are compatible with a model of rapid eye movement sleep generation in which a key element is mesopontine cholinergic input depolarizing and increasing the excitability of reticular core neurons.
大量且一致的数据表明脑桥中脑胆碱能神经元与快速眼动睡眠的产生有关，并表明许多快速眼动睡眠事件是由脑桥网状结构神经元的激活介导的。有解剖学证据表明从脑桥中脑胆碱能核向脑桥网状结构有投射，但尚无研究表明刺激该胆碱能区会在脑桥网状结构神经元中产生兴奋性突触后电位。在本研究中，对168只急性麻醉猫的脑桥网状结构神经元进行了细胞内记录，这些神经元通过延髓网状结构的逆向激活和神经生物素细胞内标记来识别。在这些神经元中评估了同侧脑桥中脑胆碱能区的外侧背侧被盖核部分的单脉冲电刺激的效应。在乌拉坦麻醉下，这种刺激在22个记录的神经元中的21个中产生了长潜伏期兴奋性突触后电位（平均 = 3毫秒），这与无髓胆碱能纤维的传导速度一致（测量的传导速度为2米/秒）。静脉注射毒蕈碱型胆碱能受体阻滞剂东莨菪碱（n = 40个神经元）以及急性切断外侧背侧被盖核与记录的神经元之间的联系（n = 40）后，这种兴奋性突触后电位几乎完全消失。相比之下，短潜伏期兴奋性突触后电位（0.7 - 1.5毫秒）的幅度并未因东莨菪碱而降低，并且在急性横断后仍可诱发。与较长潜伏期兴奋性突触后电位不同，其幅度并未因巴比妥类麻醉而降低。这些数据表明存在从兴奋性胆碱能外侧背侧被盖核向脑桥网状结构的投射，为其他表明脑桥中脑胆碱能神经元与快速眼动睡眠产生有关的证据提供了进一步支持，并且与快速眼动睡眠产生模型相符，在该模型中一个关键要素是脑桥中脑胆碱能输入使网状核心神经元去极化并增加其兴奋性。
