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介导虎螈视网膜中运动检测的神经相互作用。

Neural interactions mediating the detection of motion in the retina of the tiger salamander.

作者信息

Werblin F, Maguire G, Lukasiewicz P, Eliasof S, Wu S M

机构信息

Neurobiology Group, University of California, Berkeley 94720.

出版信息

Vis Neurosci. 1988;1(3):317-29. doi: 10.1017/s0952523800001978.

Abstract

The neural circuitry underlying movement detection was inferred from studies of amacrine cells under whole-cell patch clamp in retinal slices. Cells were identified by Lucifer yellow staining. Synaptic inputs were driven by "puffing" transmitter substances at the dendrites of presynaptic cells. Spatial sensitivity profiles for amacrine cells were measured by puffing transmitter substances along the lateral spread of their processes. Synaptic pathways were separated and identified with appropriate pre- and postsynaptic pharmacological blocking agents. Two distinct amacrine cell types were found: one with narrow spread of processes that received sustained excitatory synaptic current, the other with very wide spread of processes that received transient excitatory synaptic currents. The transient currents found only in the wide-field amacrine cell were formed presynaptically at GABAB receptors. They could be blocked with baclofen, a GABAB agonist, and their time course was extended by AVA, a GABAB antagonist. Baclofen and AVA had no direct affect upon the wide-field amacrine cell, but picrotoxin blocked a separate, direct GABA input to this cell. The narrow-field amacrine cell was shown to be GABAergic by counterstaining with anti-GABA antiserum after it was filled with Lucifer yellow. Its narrow, spatial profile and sustained synaptic input are properties that closely match those of the GABAergic antagonistic signal that forms transient activity (described above), suggesting that the narrow-field amacrine cell itself is the source of the GABAergic interaction mediating transient activity in the inner plexiform layer (IPL). Other work has shown a GABAB sensitivity at some bipolar terminals, suggesting a population of bipolars as the probable site of interaction mediating transient action. The results suggest that two local populations of amacrine cell types (sustained and transient) interact with the two populations of bipolar cell types (transient forming and nontransient forming). These interactions underlie the formation of the change-detecting subunits. We suggest that local populations of these subunits converge to form the receptive fields of movement-detecting ganglion cells.

摘要

运动检测的神经回路是通过对视网膜切片中全细胞膜片钳下无长突细胞的研究推断出来的。通过荧光黄染色来识别细胞。突触输入是通过在突触前细胞的树突处“吹入”递质物质来驱动的。无长突细胞的空间敏感性分布是通过沿着其突起的横向扩展吹入递质物质来测量的。突触通路通过适当的突触前和突触后药理学阻断剂来分离和识别。发现了两种不同类型的无长突细胞:一种突起分布狭窄,接受持续的兴奋性突触电流;另一种突起分布非常广泛,接受短暂的兴奋性突触电流。仅在广域无长突细胞中发现的短暂电流在突触前由GABAB受体形成。它们可以被GABAB激动剂巴氯芬阻断,其时间进程被GABAB拮抗剂AVA延长。巴氯芬和AVA对广域无长突细胞没有直接影响,但苦味毒阻断了该细胞单独的直接GABA输入。在用荧光黄填充后,通过抗GABA抗血清的复染显示窄域无长突细胞是GABA能的。其狭窄的空间分布和持续的突触输入与形成短暂活动的GABA能拮抗信号的特性紧密匹配(如上所述),这表明窄域无长突细胞本身就是介导内网状层(IPL)中短暂活动的GABA能相互作用的来源。其他研究表明,一些双极终末存在GABAB敏感性,这表明一群双极细胞可能是介导短暂作用的相互作用位点。结果表明,两种局部无长突细胞类型(持续型和短暂型)与两种双极细胞类型(形成短暂型和非形成短暂型)相互作用。这些相互作用是变化检测亚基形成的基础。我们认为,这些亚基的局部群体汇聚形成运动检测神经节细胞的感受野。

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