Oregon Health and Science University, Ophthalmology, Portland, Oregon, USA.
Bioessays. 2010 Jul;32(7):609-14. doi: 10.1002/bies.200900198.
For almost 30 years the ion channel that initiates the ON visual pathway in vertebrate vision has remained elusive. Recent findings now indicate that the pathway, which begins with unbinding of glutamate from the metabotropic glutamate receptor 6 (mGluR6), ends with the opening of the transient receptor potential (TRP)M1 cation channel. As a component of the mGluR6 signal transduction pathway, mutations in TRPM1 would be expected to cause congenital stationary night blindness (CSNB), and several such mutations have already been identified in CSNB families. Furthermore, expression of TRPM1 in both the retina and skin raises the possibility that a genetic link exists between certain types of visual and skin disorders.
近 30 年来，脊椎动物视觉中启动光感受器信号转导的离子通道一直难以捉摸。最近的研究结果表明，该通路始于代谢型谷氨酸受体 6（mGluR6）与谷氨酸的解离，最终导致瞬时受体电位（TRP）M1 阳离子通道的开放。作为 mGluR6 信号转导通路的一个组成部分，TRPM1 的突变预计会导致先天性静止性夜盲症（CSNB），并且已经在 CSNB 家族中发现了几种这样的突变。此外，TRPM1 在视网膜和皮肤中的表达增加了某些类型的视觉和皮肤疾病之间存在遗传联系的可能性。
