半胱氨酸串珠蛋白增强突触前钙电流
Enhancement of presynaptic calcium current by cysteine string protein.
作者信息
Chen Shan, Zheng Xu, Schulze Karen L, Morris Terry, Bellen Hugo, Stanley Elis F
机构信息
Synaptic Mechanisms Section, NINDS, NIH, Bethesda, MD 20892-4156, USA.
出版信息
J Physiol. 2002 Jan 15;538(Pt 2):383-9. doi: 10.1113/jphysiol.2001.013397.
Abstract
The isolated chick ciliary neuron calyx synapse preparation was used to test cysteine string protein (CSP) action on presynaptic N-type Ca(2+) channels. Endogenous CSP was localized primarily to secretory vesicle clusters in the presynaptic nerve terminal. Introduction of recombinant CSP into the voltage clamped terminal resulted in a prominent increase in Ca(2+) current amplitude. However, this increase could not be attributed to a change in Ca(2+) channel kinetics, voltage dependence, prepulse inactivation, or G protein inhibition but was attributed to the recruitment of dormant channels. Secretory vesicle associated endogenous CSP may play an important role in enhancing Ca(2+) channel activity at the transmitter release site.
摘要
利用分离的鸡睫状神经节神经元花萼突触标本，检测了半胱氨酸串蛋白（CSP）对突触前N型Ca(2+)通道的作用。内源性CSP主要定位于突触前神经末梢的分泌囊泡簇。将重组CSP导入电压钳制的神经末梢，导致Ca(2+)电流幅度显著增加。然而，这种增加不能归因于Ca(2+)通道动力学、电压依赖性、预脉冲失活或G蛋白抑制的变化，而是归因于休眠通道的募集。与分泌囊泡相关的内源性CSP可能在增强递质释放部位的Ca(2+)通道活性方面发挥重要作用。
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