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Coupling of L type calcium channels with ryanodine receptors in presynaptic nerve terminals

L型钙通道与突触前神经末梢兰尼碱受体的偶联

基本信息

批准号：
16500265
负责人：
ISHIBASHI Hitoshi
金额：
$ 2.37万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

The effect of potassium-induced presynaptic depolarization on spontaneous postsynaptic currents under extracellular Ca^<2+>-free conditions was investigated in mechanically dissociated rat spinal cord neurons using whole-cell patch-clamp technique. Spontaneous synaptic currents were fully inhibited by application of strychnine, indicating that they were glycinergic inhibitory postsynaptic currents (IPSCs). Elevating extracellular K^+ concentration reversibly increased that frequency of spontaneous IPSCs even in the absence of extracellular Ca^<2+>. Tetrodotoxin had no effect on the potassium-induced synaptic potentiation. The potassium-induced increase in IPSC frequency was also observed in the absence of extracellular Na^+. However, the recovery from the synaptic potentiation was markedly inhibited in the Na^+-free conditions. The potassium-induced facilitation of spontaneous IPSCs was prevented by depletion of intracellular Ca^<2+> store with thapsigargin, suggesting the contribution of Ca^<2+>-release from intracellular Ca^<2+> stores.These results reveal a novel mechanism by which potassium-induced depolarization regulates the intracellular Ca^<2+> concentration and exocytosis in presynaptic nerve terminals.

在机械分离的大鼠脊髓神经元上，采用全细胞膜片钳技术，观察了钾诱导的突触前去极化对细胞外无钙条件下自发性突触后电流的影响。士的宁可完全抑制自发性突触电流，表明其为甘氨酸能抑制性突触后电流（IPSC）。即使在缺乏细胞外Ca^<2+>的情况下，细胞外K^+浓度的升高也可逆地增加了自发IPSC的频率。河豚毒素对钾诱导的突触增强没有影响。在缺乏细胞外Na^+的情况下，也观察到钾诱导的IPSC频率增加。然而，在无Na^+条件下，突触增强的恢复受到明显抑制。用毒胡萝卜素耗竭细胞内Ca^<2+>库可阻止钾诱导的自发性IPSCs易化，提示细胞内Ca ^<2 +>库释放Ca^<2+>的作用，这些结果揭示了钾诱导的去极化调节突触前神经末梢细胞内Ca^<2+>浓度和胞吐作用的新机制。

项目成果

期刊论文数量（20）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia

DOI：
10.1038/nn1485
发表时间：
2005-07-01
期刊：
NATURE NEUROSCIENCE
影响因子：
25
作者：
Taketomi, T;Yoshiga, D;Yoshimura, A
通讯作者：
Yoshimura, A

Noradrenaline-induced cation currents in isolated rat paratracheal ganglion neurons

去甲肾上腺素诱导离体大鼠气管旁神经节神经元的阳离子电流

DOI：
发表时间：
2004
期刊：
Brain Research 1023
影响因子：
0
作者：
Umezu M;Ishibashi H;Umebayashi C;Akaike N;Ito Y
通讯作者：
Ito Y

Activation of presynaptic GABAA receptors increases spontaneous glutamate release onto noradrenergic neurons of the rat locus coeruleus

突触前 GABAA 受体的激活增加大鼠蓝斑去甲肾上腺素能神经元的自发谷氨酸释放

DOI：
发表时间：
2005
期刊：
Brain Research 1046
影响因子：
0
作者：
Koga H;Ishibashi H;Shimada H;Jang IS;Nakamura TY;Nabekura J
通讯作者：
Nabekura J

Noradrenaline-induced cation currents in isolated paratracheal ganglion neurons

去甲肾上腺素在离体气管旁神经节神经元中诱导的阳离子电流

DOI：
发表时间：
2004
期刊：
Brain Research 1023
影响因子：
0
作者：
Taketomi T.;他12名;Umezu et al.
通讯作者：
Umezu et al.

Facilitation of spontaneous glutamate release by antidepressant drugs in rat locus coeruleus

抗抑郁药物促进大鼠蓝斑自发谷氨酸释放

DOI：
发表时间：
2005
期刊：
Neuroscience Letters 274
影响因子：
0
作者：
杉原泉;Taketomi et al.;S.Rudra;M.Kimura;S.Rudra;Kazutoshi Kameda;Ishibashi et al.
通讯作者：
Ishibashi et al.