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

生理实验和计算研究被用来探索神经可塑性的某些方面。由于篇幅所限，本报告仅描述我们在脊椎动物视网膜中突触可塑性机制的研究结果，视网膜在形态上是大脑的一部分。因此，我们已经确定，从短波（波长）敏感的视锥细胞到H1型水平细胞（H1 hc）的突触与介导长λ视觉信号传递的兴奋性（符号保存）突触不同，尽管这两个突触都可能使用l -谷氨酸作为神经递质；短lambda突触以APB为激动剂，具有信号反转和电导降低的作用；以cGMP为第二信使，突触具有代谢性。此外，No（一氧化氮）在视网膜适应光时通过促进cGMP的产生参与了分子机制。这解释了短突触在黑暗适应期间处于休眠状态的事实。事实上，与蓝光相比，光适应和No对H1 hc在锐化光谱灵敏度曲线和增加接受野面积方面具有相同的作用。这些观察结果被一个电缆理论模型成功地解释了，该模型结合了短lambda突触的极性反转和电导降低的特性。

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.