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卡尔莫杜林依赖于前突触性转基因谷氨酸受体的信号传递

V O'Connor¹, O El Far, E Bofill-Cardona

¹Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.

Science (New York, N.Y.)

|November 5, 1999

概括

预突触的元类谷氨酸受体 (mGluRs) 控制神经传递. 结合和素释放G蛋白子单元,使mGluRs能够抑制刺激性神经传递.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
细胞信号传输细胞信号传输

背景情况:

预突触的元类谷氨酸受体 (mGluRs) 调节谷氨酸性神经传递.
第三组mGluRs具有涉及蛋白质相互作用的细胞内碳素终端尾部.

研究的目的:

阐明III组mGluRs调节离子电流和神经传递的机制.
为了研究calmodulin和G蛋白贝塔玛子单元在mGluR功能中的作用.

主要方法:

使用突变来破坏III组mGluRs上的calmodulin结合位.
使用calmodulin对抗剂来抑制calmodulin的功能.
评估这些操纵对G蛋白介导的离子电流调节和激发性神经传递的影响.

主要成果:

影响calmodulin结合和calmodulin抗体的突变抑制了mGluR 7.通过mGluR介导的G蛋白调节的离子电流.
卡尔莫杜林抗剂也阻止了由前突触mGluRs介导的激发性神经传递的抑制.
这些发现表明,calmodulin和G蛋白贝塔亚单元与mGluR C-tail相互排斥的结合.

结论:

已经确定了一种涉及Ca(2+) -calmodulin的突触前调制的新机制.
2+) - 卡尔莫杜林对于从III组mGluRs中释放G蛋白贝塔玛子单元至关重要.
这种释放是通过前突触mGluRs来调解谷氨酸性自身抑制所必需的.

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