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γ-氨基丁酸介导的从鲤鱼视网膜水平细胞到视锥细胞的负反馈。

GABA-mediated negative feedback from horizontal cells to cones in carp retina.

作者信息

Murakami M, Shimoda Y, Nakatani K, Miyachi E, Watanabe S

出版信息

Jpn J Physiol. 1982;32(6):911-26. doi: 10.2170/jjphysiol.32.911.

Abstract

In the isolated, perfused retina of the carp, properties of the feedback pathway from horizontal cells to cones were investigated by means of electrophysiological and neuropharmacological methods. When horizontal cells were hyperpolarized by illumination with an annulus, a depolarizing synaptic potential was produced in cones at the center of the annulus, suggesting that horizontal cells receive inputs from cones and exert a negative feedback to cones. On the other hand, a hyperpolarization (EPSP) was induced in horizontal cells by application of a transretinal current pulse, which activated the release of transmitter from the photoreceptor terminals. The IPSP was abolished when the retina was perfused with a GABA-containing Ringer solution, because of desensitization of the feedback synapse. GABA also hyperpolarized the cone membrane, indicating the presence of a GABA-sensitive site in the cone. These results suggest that the GABA-mediated negative feedback operates from horizontal cells to cones in the dark, and ceases its function in the light.

摘要

在离体灌注的鲤鱼视网膜中,运用电生理和神经药理学方法研究了从水平细胞到视锥细胞的反馈通路特性。当用环形光照射使水平细胞超极化时,在环形光中心的视锥细胞中产生了去极化突触电位,这表明水平细胞接收视锥细胞的输入并对视锥细胞施加负反馈。另一方面,通过施加跨视网膜电流脉冲在水平细胞中诱导出超极化(兴奋性突触后电位),该电流脉冲激活了光感受器终末的递质释放。当视网膜用含γ-氨基丁酸(GABA)的林格液灌注时,抑制性突触后电位消失,这是由于反馈突触脱敏所致。GABA也使视锥细胞膜超极化,表明视锥细胞中存在GABA敏感位点。这些结果提示,GABA介导的负反馈在黑暗中从水平细胞作用于视锥细胞,并在光照时停止其功能。

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