Stern M, Ganetzky B
Laboratory of Genetics, University of Wisconsin, Madison 53706.
J Neurogenet. 1992 Sep;8(3):157-72. doi: 10.3109/01677069209083445.
On the basis of behavioral interactions with mutations in a potassium channel gene of Drosophila--Shaker (Sh)--we have isolated mutations in a new gene called inebriated (ine). In a wildtype background, ine mutants display no observable behavioral defects. However, in a Sh mutant background, ine mutations cause downturned wings and an indented thorax. This distinctive phenotype is also exhibited by flies of other genotypes that cause extreme neuronal hyperexcitability. We utilized the potassium channel blocking drugs quinidine and dideoxy forskolin (DDF) to test the effects of ine on synaptic transmission. DDF and ine mutations each potentiated the effects of quinidine on synaptic transmission, but neither had any observable effects in the absence of quinidine. Application of DDF to ine mutants had no effects either in the presence or absence of quinidine. We conclude that ine mutations increase neuronal membrane excitability and perhaps block a DDF-sensitive potassium channel.
基于对果蝇钾通道基因——震颤基因（Sh）突变体的行为学相互作用研究，我们分离出了一个名为沉醉基因（ine）的新基因突变体。在野生型背景下，ine突变体未表现出可观察到的行为缺陷。然而，在Sh突变体背景下，ine突变会导致翅膀下垂和胸部凹陷。其他导致神经元极度兴奋的基因型果蝇也表现出这种独特的表型。我们使用钾通道阻断药物奎尼丁和双脱氧福司可林（DDF）来测试ine对突触传递的影响。DDF和ine突变均增强了奎尼丁对突触传递的作用，但在没有奎尼丁的情况下两者均未产生任何可观察到的影响。在有或没有奎尼丁的情况下，将DDF应用于ine突变体均无效果。我们得出结论，ine突变会增加神经元膜兴奋性，并且可能阻断了一种对DDF敏感的钾通道。
