Singaram Vinod K, Morgan Philip G, Sedensky Margaret M
Department of Genetics; Case Western Reserve University; Cleveland, OH USA.
Worm. 2012;1(3):164-169. doi: 10.4161/worm.20002.
One hundred and sixty five years have passed since the first documented use of volatile anesthetics to aid in surgery, but we have yet to understand the underlying mechanism of action of these drugs. There is no question that, in vitro, volatile anesthetics can affect the function of numerous neuronal and non-neuronal proteins. In fact, volatile anesthetics are capable of binding such diverse proteins as albumin and bacterial luciferase. The promiscuity of volatile anesthetic binding makes it difficult to determine which proteins are modulated by anesthetics to cause the state of anesthesia. Consequently, despite a great deal of in vitro data, the fundamental physiological process that volatile anesthetics perturb to effect neuronal silencing is not yet identified. Recently, data has increasingly indicated that membrane leak channels may play a role in the anesthetic response. Here we comment on the use of optogenetics to further support such a model.
自首次有文献记载使用挥发性麻醉剂辅助手术以来，已经过去了165年，但我们尚未了解这些药物的潜在作用机制。毫无疑问，在体外，挥发性麻醉剂能够影响众多神经元和非神经元蛋白质的功能。事实上，挥发性麻醉剂能够与诸如白蛋白和细菌荧光素酶等多种不同的蛋白质结合。挥发性麻醉剂结合的杂乱性使得难以确定哪些蛋白质受到麻醉剂的调节从而导致麻醉状态。因此，尽管有大量的体外数据，但挥发性麻醉剂扰乱以实现神经元沉默的基本生理过程尚未被确定。最近，越来越多的数据表明膜漏通道可能在麻醉反应中起作用。在此，我们评论利用光遗传学进一步支持这样一种模型。
