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Inositol 1,4,5-trisphosphate receptors (IP 3 R) are Ca 2+  channels on the neuronal endoplasmic reticulum (ER) membrane. They are gated by IP 3 , produced upon external stimulation and activation of G protein-coupled receptors on the plasma membrane (PM). IP 3 -mediated Ca 2+  release, and the resulting depletion of the ER store, triggers entry of extracellular Ca 2+  by store-operated Ca 2+  entry (SOCE). Mutations in IP 3 R attenuate SOCE. Compromised IP 3 R function and SOCE during pupal development of  Drosophila  leads to flight deficits and mimics suppression of neuronal activity during pupal or adult development. To understand the effect of compromised IP 3 R function on pupal neuronal calcium signaling, we examined the effects of mutations in the IP 3 R gene ( itpr ) on Ca 2+  signals in cultured neurons derived from  Drosophila  pupae. We observed increased spontaneous Ca 2+  influx across the PM of isolated pupal neurons with mutant IP 3 R and also a loss of SOCE. Both spontaneous Ca 2+  influx and reduced SOCE were reversed by over-expression of  dOrai  and  dSTIM , which encode the SOCE Ca 2+  channel and the ER Ca 2+ -sensor that regulates it, respectively. Expression of voltage-gated Ca 2+  channels ( cac, Ca-α1D  and  Ca-αT ) was significantly reduced in  itpr  mutant neurons. However, expression of  trp  mRNAs and transient receptor potential (TRP) protein were increased, suggesting that TRP channels might contribute to the increased spontaneous Ca 2+  influx in neurons with mutant IP 3 R. Thus, IP 3 R/SOCE modulates spontaneous Ca 2+  influx and expression of PM Ca 2+  channels in  Drosophila  pupal neurons. Spontaneous Ca 2+  influx compensates for the loss of SOCE in  Drosophila   itpr  mutant neurons.

Spontaneous Ca2+ Influx in Drosophila Pupal Neurons Is Modulated by IP3-Receptor Function and Influences Maturation of the Flight Circuit