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运动神经末梢的高渗性神经分泌是一个钙依赖过程吗?

Is hyperosmotic neurosecretion from motor nerve endings a calcium-dependent process?

作者信息

Shimoni Y, Alnaes E, Rahamimoff R

机构信息

Department of Physiology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

出版信息

Nature. 1977 May 12;267(5607):170-2. doi: 10.1038/267170a0.

DOI:10.1038/267170a0
PMID:16073435
Abstract

Spontaneous liberation of neurotransmitter quanta is strongly affected by the osmotic pressure of the extracellular fluid. Elevation of the osmolarity by 20-30% increases the rate of release from motor nerve endings by more than one order of magnitude. In this respect the neuromuscular junction resembles some other secretory systems. The mechanism of this hyperosmotic neurosecretion is not yet understood; extracellular calcium ions are not directly responsible, since this effect can be produced in their absence. Recently, it has been suggested that the liberation of neurotransmitter is regulated by the intracellular concentration of free calcium ions. We have therefore examined the hypothesis that hyperosmotic neurosecretion originates from an increase in internal calcium concentration ([Ca]in). At the frog neuromuscular synapse however, it is impossible at present to estimate directly free [Ca]in; hence we used an indirect technique, which is based on two assumptions; first, the frequency of the miniature endplate potentials (m.e.p.p.s.) reflects free [Ca]in. Second, the movement of calcium ions across the presynaptic membrane is governed by the electrochemical gradient, and by the calcium conductance (g(Ca)). If hyperosmotic neurosecretion is caused by an increase in [Ca]in, then increasing g(Ca), under reversed electrochemical gradient for the calcium should cause a reduction in the effect of hyperosmotic stress on transmitter release. We report that hyperosmotic neurosecretion is dependent on [Ca]in.

摘要

神经递质量子的自发释放受到细胞外液渗透压的强烈影响。渗透压升高20%-30%会使运动神经末梢的释放速率增加一个多数量级以上。在这方面,神经肌肉接头类似于其他一些分泌系统。这种高渗性神经分泌的机制尚不清楚;细胞外钙离子并非直接原因,因为在没有钙离子的情况下也能产生这种效应。最近,有人提出神经递质的释放受细胞内游离钙离子浓度的调节。因此,我们检验了高渗性神经分泌源于细胞内钙浓度([Ca]in)增加的假说。然而,在青蛙神经肌肉突触处,目前无法直接估计游离的[Ca]in;因此,我们采用了一种间接技术,该技术基于两个假设:第一,微小终板电位(m.e.p.p.s.)的频率反映游离的[Ca]in。第二,钙离子跨突触前膜的移动受电化学梯度和钙电导(g(Ca))的控制。如果高渗性神经分泌是由[Ca]in增加引起的,那么在钙离子的电化学梯度反转的情况下增加g(Ca),应该会导致高渗应激对递质释放的影响降低。我们报告高渗性神经分泌依赖于[Ca]in。

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Readily releasable pool size changes associated with long term depression.
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J Physiol. 1995 Feb 1;482 ( Pt 3)(Pt 3):511-20. doi: 10.1113/jphysiol.1995.sp020536.
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