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虎螈视网膜中的一条三神经元去抑制通路促进了对变化的反应。

Response to change is facilitated by a three-neuron disinhibitory pathway in the tiger salamander retina.

作者信息

Roska B, Nemeth E, Werblin F S

机构信息

Division of Neurobiology, Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720, USA.

出版信息

J Neurosci. 1998 May 1;18(9):3451-9. doi: 10.1523/JNEUROSCI.18-09-03451.1998.

DOI:10.1523/JNEUROSCI.18-09-03451.1998
PMID:9547252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6792670/
Abstract

Most retinal ganglion cells respond only transiently, for approximately 150 msec at the onset and termination of a light flash. The responses are transient because it has been shown that bipolar-to-ganglion cell transmission is truncated after 150 msec by a feedback inhibition to bipolar cell terminals. The feedback inhibition itself must be delayed by approximately 150 msec to allow the initial bipolar-ganglion cell transmission. This study identifies a three-component serial synaptic pathway from glycinergic amacrine cells to GABAergic amacrine cells to bipolar cell terminals as one source of this delay. We used perforated and whole-cell patch-clamp recordings to measure the timing of light responses in amacrine, bipolar, and ganglion cells under control and glycine and GABA receptor-blocked conditions. Our results suggest that, after a light flash, a population of glycinergic amacrine cells responds first, inhibiting a population of GABAergic amacrine cells for approximately 150 msec. The GABAergic amacrine cells feed back to bipolar terminals, but only after the 150 msec delay, allowing the bipolar terminals to excite ganglion cells for the first 150 msec. Blocking the glycinergic amacrine cell activity with strychnine allows the GABAergic system to become active earlier. GABAergic amacrine cells then inhibit release from bipolar cells earlier. Under these conditions, the ganglion cell response to change would be decreased.

摘要

大多数视网膜神经节细胞仅产生短暂反应,在光闪光开始和结束时约持续150毫秒。这些反应是短暂的,因为已经表明双极细胞向神经节细胞的传递在150毫秒后会因双极细胞终末的反馈抑制而截断。反馈抑制本身必须延迟约150毫秒,以允许最初的双极 - 神经节细胞传递。本研究确定了一条从甘氨酸能无长突细胞到GABA能无长突细胞再到双极细胞终末的三成分串联突触通路,作为这种延迟的一个来源。我们使用穿孔膜片钳和全细胞膜片钳记录来测量在对照以及甘氨酸和GABA受体阻断条件下无长突细胞、双极细胞和神经节细胞光反应的时间。我们的结果表明,在光闪光后,一群甘氨酸能无长突细胞首先做出反应,抑制一群GABA能无长突细胞约150毫秒。GABA能无长突细胞反馈到双极终末,但仅在延迟150毫秒之后,从而使双极终末在最初的150毫秒内能够兴奋神经节细胞。用士的宁阻断甘氨酸能无长突细胞的活动会使GABA能系统更早地活跃起来。然后GABA能无长突细胞会更早地抑制双极细胞的释放。在这些条件下,神经节细胞对变化的反应会减弱。

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