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