低钙诱导增强脊椎动物视网膜中从光感受器到水平细胞的化学突触传递。
Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.
作者信息
Piccolino M, Byzov A L, Kurennyi D E, Pignatelli A, Sappia F, Wilkinson M, Barnes S
机构信息
Dipartimento di Biologia, Università di Ferrara, Italy.
出版信息
Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2302-6. doi: 10.1073/pnas.93.6.2302.
According to the classical calcium hypothesis of synaptic transmission, the release of neurotransmitter from presynaptic terminals occurs through an exocytotic process triggered by depolarization-induced presynaptic calcium influx. However, evidence has been accumulating in the last two decades indicating that, in many preparations, synaptic transmitter release can persist or even increase when calcium is omitted from the perfusing saline, leading to the notion of a "calcium-independent release" mechanism. Our study shows that the enhancement of synaptic transmission between photoreceptors and horizontal cells of the vertebrate retina induced by low-calcium media is caused by an increase of calcium influx into presynaptic terminals. This paradoxical effect is accounted for by modifications of surface potential on the photoreceptor membrane. Since lowering extracellular calcium concentration may likewise enhance calcium influx into other nerve cells, other experimental observations of "calcium-independent" release may be reaccommodated within the framework of the classical calcium hypothesis without invoking unconventional processes.
根据经典的突触传递钙假说，神经递质从突触前终末的释放是通过去极化诱导的突触前钙内流触发的胞吐过程发生的。然而，在过去二十年中，越来越多的证据表明，在许多标本中，当灌注盐水中不含钙时，突触递质释放仍可持续甚至增加，这导致了“钙非依赖性释放”机制的概念。我们的研究表明，低钙培养基诱导的脊椎动物视网膜光感受器与水平细胞之间突触传递的增强是由突触前终末钙内流增加引起的。这种矛盾的效应是由光感受器膜表面电位的改变所解释的。由于降低细胞外钙浓度同样可能增强钙流入其他神经细胞，因此“钙非依赖性”释放的其他实验观察结果可能无需引入非常规过程即可在经典钙假说的框架内重新解释。
Zotero 插件