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瞬态开/关神经节细胞反应的时间结构及其与视网膜内处理的关系。

The temporal structure of transient ON/OFF ganglion cell responses and its relation to intra-retinal processing.

作者信息

Thiel Andreas, Greschner Martin, Ammermüller Josef

机构信息

Neurobiology, Carl von Ossietzky University Oldenburg, Oldenburg, Germany.

出版信息

J Comput Neurosci. 2006 Oct;21(2):131-51. doi: 10.1007/s10827-006-7863-x. Epub 2006 May 26.

Abstract

A subpopulation of transient ON/OFF ganglion cells in the turtle retina transmits changes in stimulus intensity as series of distinct spike events. The temporal structure of these event sequences depends systematically on the stimulus and thus carries information about the preceding intensity change. To study the spike events' intra-retinal origins, we performed extracellular ganglion cell recordings and simultaneous intracellular recordings from horizontal and amacrine cells. Based on these data, we developed a computational retina model, reproducing spike event patterns with realistic intensity dependence under various experimental conditions. The model's main features are negative feedback from sustained amacrine onto bipolar cells, and a two-step cascade of ganglion cell suppression via a slow and a fast transient amacrine cell. Pharmacologically blocking glycinergic transmission results in disappearance of the spike event sequence, an effect predicted by the model if a single connection, namely suppression of the fast by the slow transient amacrine cell, is weakened. We suggest that the slow transient amacrine cell is glycinergic, whereas the other types release GABA. Thus, the interplay of amacrine cell mediated inhibition is likely to induce distinct temporal structure in ganglion cell responses, forming the basis for a temporal code.

摘要

乌龟视网膜中存在一类瞬态开/关神经节细胞亚群,它们以一系列不同的尖峰事件来传递刺激强度的变化。这些事件序列的时间结构系统地依赖于刺激,因此携带了有关先前强度变化的信息。为了研究尖峰事件在视网膜内的起源,我们进行了细胞外神经节细胞记录以及水平细胞和无长突细胞的同步细胞内记录。基于这些数据,我们开发了一个计算视网膜模型,该模型在各种实验条件下能再现具有逼真强度依赖性的尖峰事件模式。该模型的主要特征包括持续无长突细胞对双极细胞的负反馈,以及通过慢速和快速瞬态无长突细胞对神经节细胞进行两步级联抑制。药理学上阻断甘氨酸能传递会导致尖峰事件序列消失,如果单一连接(即慢速瞬态无长突细胞对快速瞬态无长突细胞的抑制)被削弱,该模型就能预测到这种效应。我们认为慢速瞬态无长突细胞是甘氨酸能的,而其他类型释放γ-氨基丁酸。因此,无长突细胞介导的抑制作用之间的相互作用可能会在神经节细胞反应中诱导出独特的时间结构,形成时间编码的基础。

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