课题基金 / 基金详情

Identification of synapse pairs between neurons in the basal forebrain nuclei

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
批准号:
11680808
负责人:
MOMIYAMA Toshihiko
金额:
$2.37万
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
项目状态:
已结题
起止时间:
1999 至 2000

项目摘要

项目成果

MOMIYAMA Toshihiko的其他基金

相关文献

中文摘要
翻译
采用10-14日龄大鼠含基底前脑核(BF)的脑切片。对BF内视觉识别的大(bbb25 μm)和小(<15 μm)神经元进行成对全细胞记录。大神经元的电生理特性与文献报道一致,被认为是胆碱能神经元。当通过记录移液管对小神经元施加去极化脉冲时,在10%的记录对中,大神经元中诱发了突触电流。10 μM双球茎碱阻断了诱发的突触电流,提示小神经元具有gaba能。单独的一系列形态学研究表明,含有生长抑素的gaba能神经元与胆碱能神经元之间存在突触接触,表明这两类神经元之间存在功能相互作用。投射到BF的腹侧被盖多巴胺能神经元的神经元活动受皮层或脑干谷氨酸输入的调节。利用片膜片钳技术阐明了多巴胺诱导的非nmda谷氨酸能突触传递到多巴胺能神经元的调节。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样多巴胺受体,其激活通过减少Ca^<2+>内流抑制谷氨酸释放(Koga & Momiyama, 2000)。在形态和功能方面,BF常与纹状体相比较。研究了gaba能突触传递及其在纹状体胆碱能中间神经元中的多巴胺调节作用。结果表明,GABA能末端d_2样受体的激活选择性地阻断n型以减少GABA的释放。这是首次发现Ca^<2+>通道亚型不参与突触前多巴胺受体介导的突触传递调节(Momiyama & Koga, 2001)。
英文摘要
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).
期刊论文(5)
专著(0)
科研奖励(0)
会议论文
Momiyama,T.(分担執筆): "Slow synaptic responses and modulation"Springer-Verlag Tokyo. 455 (2000)
Momiyama, T.(撰稿人):“缓慢的突触反应和调制”Springer-Verlag Tokyo 455 (2000)。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Momiyama, T.: "Function of monoamines and peptide in the vestibular complex"Equilibrium Research. 59(1). 1-8 (2000)
Momiyama,T.:“前庭复合体中单胺和肽的功能”平衡研究。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Momiyama, T.: "Dopamine-induced presynaptic modulation of excitatory and inhibitory transmission in the central nervous system."In : Slow synaptic responses and modulation, edited by Kuba, H.et al., Springer-Verlag Tokyo. 410-415 (2000)
Momiyama, T.:“多巴胺诱导的中枢神经系统兴奋性和抑制性传递的突触前调节”。载于:缓慢的突触反应和调节,由 Kuba, H. 等人编辑,东京 Springer-Verlag。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Analysis of dynamic interaction between dopamine receptors and calcium channels located on the synaptic terminals in the basal forebrain
  • 批准号:
    21500374
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.83万
  • 财政年份:
    2009
  • 负责人:
    MOMIYAMA Toshihiko
  • 依托单位:
Analyses of interaction among neurons in the basal forebrain and its developmental changes
Invivoパッチクランプ法を用いた線条体シナプス伝達機構の解析
Analysis of function of dopamine as a retrograde messenger in the basal ganglia