Abstract
Coordinated flight in winged insects requires rhythmic activity of the underlying neural circuit. Here, we show that Drosophila mutants for the inositol 1,4,5-trisphosphate (InsP(3)) receptor gene (itpr) are flightless. Electrophysiological recordings from thoracic indirect flight muscles show increased spontaneous firing accompanied by a loss of rhythmic flight activity patterns normally generated in response to a gentle puff of air. In contrast, climbing speed, the jump response, and electrical properties of the giant fiber pathway are normal, indicating that general motor coordination and neuronal excitability are much less sensitive to itpr mutations. All mutant phenotypes are rescued by expression of an itpr(+) transgene in serotonin and dopamine neurons. Pharmacological and immunohistochemical experiments support the idea that the InsP(3) receptor functions to modulate flight specifically through serotonergic interneurons. InsP(3) receptor action appears to be important for normal development of the flight circuit and its central pattern generator.
