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Exploration of plasticity visual physiologic functions by simultaneous studies on artificial neural networks and vertebrate retina

人工神经网络与脊椎动物视网膜同步研究探索可塑性视觉生理功能

基本信息

批准号：
05452404
负责人：
YASUI Syozo
金额：
$ 3.46万
依托单位：
Kyushu Institute of Technology
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05452404/
关键词：
Retina Horizontal Cell Synapse Glutamate Neural Network Data Compression-Recovery Plasticity NO 情報圧縮情報復元

项目摘要

Physiological experiments as well as computational studies were conducted to explore certain aspects of the neural plasticity. Due to the lack of space, this report only describes our results concerned with synaptic plasticity mechanisms in the vertebrate retina which morphogenetically is a part of the brain. Thus, we have established that the synapse from short-lambda (wavelength) sensitive cones to H1 type horizontal cells (H1 HCs) is different from the excitatory (sign-conserving) synapse mediating the long-lambda visual signal transmission, althogh both synapses presumablly use L-glutamate as the neurotransmitter ; the short-lambda synapse is sigh-inverting and conductance-decreasing with APB as an agonist, and the synapse is metabotropic with cGMP as the second messenger. Furthermore, No (nitric oxide) is involved in the molecular mechanism, by facilitating the cGMP production when the retina is light adapted. This explains the fact that the short-lambda synapse is dormant during dark adaptation. In fact, light adaptaion and No have the same effects on H1 HCs in sharpening the spectral sensitivity curve and increasing the receptive field size for red than blue lights. These observations were succesfully accounted for by a cable theory model incorporating the polarity-inverting and conductance-decreasing properties of the short-lambda synapse.

生理实验以及计算研究进行了探索神经可塑性的某些方面。由于篇幅所限，本文仅描述我们在脊椎动物视网膜中的突触可塑性机制，而视网膜在形态发生上是大脑的一部分。因此，我们已经确定，短λ的突触H1型水平细胞（H1 HCs）的（波长）敏感视锥不同于兴奋性视锥，（符号保存）突触介导长λ视觉信号传递，尽管两个突触都可能使用L-谷氨酸作为神经递质;短λ突触是信号倒置和电导降低的突触，以APB为激动剂，该突触是代谢性的，cGMP为第二信使。此外，NO（一氧化氮）参与分子机制，当视网膜适应光时促进cGMP的产生。这解释了短λ突触在暗适应期间处于休眠状态的事实。事实上，光适应和NO对H1毛细胞具有相同的作用，使其对红光的光谱敏感性曲线变尖，并使其感受野的大小比蓝光大。这些观察结果成功地占电缆理论模型纳入极性反转和电导降低属性的短λ突触。