Identification of synapse pairs between neurons in the basal forebrain nuclei

前脑基底核神经元之间突触对的识别

基本信息

批准号：
11680808
负责人：
MOMIYAMA Toshihiko
金额：
$ 2.37万
依托单位：
Okazaki National Research Institute
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

项目摘要

Brain slices containing basal forebrain nuclei (BF) obtained from 10-14 day-old rats were used. Paired whole-cell recordings were made from visually identified large (>25 μm) and small (<15 μm) neurons within the BF.Large neurons were identified as cholinergic since their electrophysiological properties conformed to the reported ones. When a depolarizing pulse was applied to the small neuron through the recording pipette, a synaptic current was evoked in the large neurone in 10 % of the recorded pairs. The evoked synaptic currents were blocked by bicuculline (10 μM), suggesting that the small neurons are GABAergic. The separate series of morphological studies have clarified that somatostatin-containing GABAergic neurons make synaptic contacts with cholinergic neurons, indicating the existence of functional interactions between these two types of neurons.Neuronal activities of ventral tegmental dopaminergic neurons which project to the BF are regulated by glutamatergic inputs fro cortex or brain stem. Dopamine-induced modulation of non-NMDA glutamatergic synaptic transmission onto dopaminergic neurons was elucidated using slice patch-clamp technique. The findings suggest that afferent glutamatergic fibers terminating dopaminergic neurons possess presynaptic D_2-like dopamine receptors, activation of which inhibits glutamate release by reducing Ca^<2+> influx (Koga ＆ Momiyama, 2000).BF is often compared with striatum in both morphological and functional aspects. GABAergic synaptic transmission and its modulation by dopamine in striatal cholinergic interneurons were also investigated. The results suggest that activation of D_2-like receptors in the GABAergic terminals selectively block N-type to reduce GABA release. Thus is the first report that identified the Ca^<2+> channel subtype unvolved in presynaptic dopamine receptor-mediated modulation of synaptic transmission (Momiyama ＆ Koga, 2001).

使用了含有从10-14天大大鼠获得的基本前脑核（BF）的脑切片。配对的全细胞记录是由视觉上鉴定出的大（>25μm）和BF内的小（<15μM）神经元制成的，因为它们的电生理特性符合报告的神经生理特性。当通过记录移液移移移移移移移移移感向小型神经元应用推出脉冲时，在记录的10％的大神经元中唤起了突触电流。诱发的突触电流被双瓜氨酸（10μM）阻塞，表明小神经元是GABA能。一系列单独的形态研究已经澄清了，含有生长抑素的GABA能神经元与胆碱能神经元之间的突触接触，表明这两种神经元之间存在功能相互作用。腹侧割伤性多巴胺剂神经元的神经元之间的非神经元活性通过BF调节的牙齿填充孔孔或大脑填充孔被调节。使用切片贴片钳技术阐明了多巴胺诱导的非NMDA谷氨酸能突触传播到多巴胺能神经元上的调节。研究结果表明，终止多巴胺能神经元的传入谷氨酸能纤维具有突触前D_2类样的多巴胺受体，这些受体的激活通过减少Ca^<2+>影响而抑制谷氨酸能释放（Koga＆Momiyama，2000）.bf与STRITAIN中的功能相比，还研究了GABA能突触传播及其在纹状体胆碱能中间神经元中的调节。结果表明，GABA能末端中D_2样受体的激活有选择地阻断N型以减少GABA释放。这是第一个鉴定出在突触前多巴胺受体介导的突触传播调节中未verved的CA^<2+>通道亚型的报告（Momiyama＆Koga，2001）。