We investigated the neuromuscular transmission in relation with genetic neuronal excitability changes in mutantsT(X;Y)V7andShKS133ofDrosophila.These mutations affect two different genes belonging to theShakergene complex which encode different yet functionally related proteins. Experiments were performed on neuromuscular junctions fromDrosophilalarvae by recording pre- and postsynatic membrane currents using external electrodes. It was found that the neuromuscular electrophysiological phenotype ofT(X;Y)V7is caused by presynaptic membrane hyperexcitability probably in relation with a Ca2+-dependent down regulation of voltage dependent K channels. By contrast, theShKS133phenotype can be explained solely by action potential widening due to the absence of type-A K channels.