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 (InsP3) 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 InsP3 receptor functions to modulate flight specifically through serotonergic interneurons. InsP3 receptor action appears to be important for normal development of the flight circuit and its central pattern generator.
Loss of Flight and Associated Neuronal Rhythmicity in Inositol 1,4,5-Trisphosphate Receptor Mutants of Drosophila
Santanu Banerjee,Jisue Lee,K. Venkatesh,Chun-Fang Wu,G. Hasan
Published 2004 in Journal of Neuroscience
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PUBLICATION RECORD
- Publication year
2004
- Venue
Journal of Neuroscience
- Publication date
2004-09-08
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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