首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.
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Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

机译:低钙诱导的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的增强。

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摘要

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.
机译:根据突触传递的经典钙假说,神经递质从突触前末端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而发生的。然而,在过去的二十年中,越来越多的证据表明,在许多制剂中,当从灌注盐水中省略钙时,突触递质的释放可以持续甚至增加,从而导致“钙非依赖性释放”机制的概念。我们的研究表明,低钙介质诱导的脊椎动物视网膜感光细胞和水平细胞之间的突触传递增强是由于钙向突触前末端的流入增加所致。这种矛盾的作用是由于感光膜上表面电位的改变而引起的。由于降低细胞外钙浓度可能同样会增加钙向其他神经细胞的流入,因此可以在经典钙假设的框架内重新进行“钙非依赖性”释放的其他实验观察,而无需进行非常规过程。

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