斯克里普斯研究所科学家确定了1个特殊基因能让夜视成为可能。研究集中在 nyctalopin 基因上，它的突变体导致遗传性夜盲症，患者在弱光环境下视力急剧下低。相关研究发表在8月10日的神经科学期刊上。
从老鼠视网膜中找到夜盲症的“元凶”
斯克里普斯研究所副教授Kirill Martemyanov称，截止到目前，我们对视觉信号通路中 nyctalopin 基因功能的了解还是很有限。该基因的视觉功能首次被发现，我们还找到它与弱光下支持视力的大分子复合物之间的关系。
视觉触发的初始条件是光子击中视网膜上感光细胞。接受光子后，感光细胞产生一个快速向下游神经元传递的反应。下游神经元接受信号后，将信号传递到大脑中，最终形成视觉图像。
Martemyanov解释道，视杆细胞和双极细胞之间存在一类特殊的突触，它们在视觉信号传导过程中发挥非常关键作用。视杆细胞对光产生反应但不能正常地传递信号，夜视障碍就会出现。缺少传递的信号，我们将在一半的时间内不适应地生存在黑暗环境中。
在新的研究中，科学家在小鼠视网膜中筛选夜盲蛋白质。该编码基因作为夜盲症的首要诱因已经知道10年了，但该基因的功能一直是个谜。新研究表明：夜盲基因表达的蛋白是一类分子黏合剂用于把突触中信号传导复合物的关键组分黏合在一起，从而实现感光信号的快速和完整地传输。（生物探索译 Pobee）
生物探索推荐英文摘要
TRPM1 Forms Complexes with Nyctalopin In Vivo and Accumulates in Postsynaptic Compartment
of ON-Bipolar Neurons in mGluR6-Dependent Manner
Abstract：Synaptic transmission between light-sensory photoreceptor cells and downstream ON-bipolar neurons plays an important role for vertebrate vision. This process is mediated by the G-protein-coupled receptor pathway involving glutamate receptor mGluR6 and effector channel TRPM1. The signal transmission occurs on a rapid timescale; however, the molecular organization that ensures timely signaling in this cascade is unknown. Genetic studies in human patients and animal models reveal that ON-bipolar cell signaling depends on the synaptic protein nyctalopin. We have conducted a proteomic search for proteins associated with nyctalopin in the mouse retina and identified TRPM1 as the binding partner. We further demonstrate that nyctalopin additionally interacts with mGluR6 receptor. Disruption of mGluR6 prevented targeting of TRPM1 to the postsynaptic compartment of ON-bipolar neurons. These results reveal a unique macromolecular organization of the mGluR6 cascade, where principal signaling components are scaffolded by nyctalopin, creating an organization essential for the correct localization of the signaling ensemble and ultimately intact transmission of the signal at the first visual synapse.
