Stern M, Ganetzky B
Laboratory of Genetics, University of Wisconsin, Madison 53706.
J Neurogenet. 1989 Aug;5(4):215-28. doi: 10.3109/01677068909066209.
Synaptic transmission in Drosophila can be altered by mutations in specific genes. For example, mutations in the Shaker (Sh) gene, which encodes the rapidly inactivating A-type potassium channel, cause repetitive nerve firing and prolonged transmitter release at the neuromuscular junction. Here we show that mutations in the Hyperkinetic (Hk) gene also affect the properties of synaptic transmission at the neuromuscular junction. In particular, we find that whereas single or low frequency nerve stimulation evokes a wild type postsynaptic response, at higher frequencies of nerve stimulation, each stimulus results in repetitive nerve firing and increased postsynaptic response, which is similar to that observed in Sh mutants. Various experiments suggest that this increased postsynaptic response results from prolonged depolarization of the nerve terminal, leading to increased transmitter release at the neuromuscular junction. The similarity in phenotypes between Sh and Hk mutants, along with the observation that Sh is epistatic to Hk in its effects on synaptic transmission, suggest that Hk acts on synaptic transmission by an effect on A-type potassium channels.
果蝇中的突触传递可因特定基因突变而改变。例如，编码快速失活的A 型钾通道的“颤抖”（Shaker，Sh）基因突变会导致神经重复放电以及神经肌肉接头处递质释放延长。在此我们表明，“运动亢进”（Hyperkinetic，Hk）基因突变也会影响神经肌肉接头处的突触传递特性。具体而言，我们发现，虽然单次或低频神经刺激会引发野生型的突触后反应，但在较高频率的神经刺激下，每次刺激都会导致神经重复放电以及突触后反应增强，这与在Sh突变体中观察到的情况相似。各种实验表明，这种增强的突触后反应是由神经末梢的去极化延长所致，从而导致神经肌肉接头处递质释放增加。Sh和Hk突变体表型的相似性，以及Sh在对突触传递的影响上对Hk呈上位性这一观察结果，表明Hk通过对A 型钾通道的作用来影响突触传递。
