We have identified a new gene inDrosophilaon the basis of a mutation that affects both behavior and neuronal excitability. This mutation, calledbemused (bem)is the result of a P element insertion at cytological position 85D. Flies defective atbemdisplay greatly reduced coordination, flight ability and fertility. Thebemmutation also affects synaptic transmission at the larval neuromuscular junction. In particular,bemlarvae display a more rapid onset of augmentation thanbem+larvae. This effect is potentiated by the potassium channel blocking drug quinidine. The increased transmitter release that occurs inbemmutants following repetitive nerve stimulation is accompanied by the appearance of extra action potentials in the motor neuron. We conclude that thebemmutation increases neuronal excitability, possibly as a result of a defect in an ion channel structural or regulatory gene.