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Calcium (Ca2+) signaling is known to regulate the development, maintenance and modulation of activity in neuronal circuits that underlie organismal behavior. In Drosophila, intracellular Ca2+ signaling by the inositol 1,4,5-trisphosphate receptor and the storeoperated channel (dOrai) regulates the formation and function of neuronal circuits that control flight. Here, we show that restoring InsP3R activity in insulin-producing neurons of flightless InsP3R mutants (itpr) during pupal development can rescue systemic flight ability. Expression of the store operated Ca2+ entry (SOCE) regulator dSTIM in insulin-producing neurons also suppresses compromised flight ability of InsP3R mutants suggesting that SOCE can compensate for impaired InsP3R function. Despite restricted expression of wild-type InsP3R and dSTIM in insulin-producing neurons, a global restoration of SOCE and store Ca2+ is observed in primary neuronal cultures from the itpr mutant. These results suggest that restoring InsP3R-mediated Ca2+ release and SOCE in a limited subset of neuromodulatory cells can influence systemic behaviors such as flight by regulating intracellular Ca2+homeostasis in a large population of neurons through a non-cell-autonomous mechanism. [ABSTRACT FROM AUTHOR]