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The Journal of Neuroscience, September 8, 2004, 24(36):7869-7878; doi:10.1523/JNEUROSCI.0656-04.2004

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Cellular/Molecular
Loss of Flight and Associated Neuronal Rhythmicity in Inositol 1,4,5-Trisphosphate Receptor Mutants of Drosophila

Santanu Banerjee,¹ Jisue Lee,² K. Venkatesh,¹ Chun-Fang Wu,² and Gaiti Hasan¹

¹National Centre for Biological Sciences, Tata Institute of Fundamental Research, Gandhi Krishi Vigyan Kendra Campus, Bangalore 560065, India, and ²Department of Biological Sciences, University of Iowa, Iowa City, Iowa 52242

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.

Key words: calcium; aminergic; serotonin; central pattern generator; inositol 1,4,5-triphosphate receptor; flight

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Received Feb 24, 2004; revised July 23, 2004; accepted July 28, 2004.

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