Neurobiological research of the brain mechanisms controlling insect sexual behavior

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The Drosophila painless (pain) gene encodes a transient receptor potentialion channel. First, we identified that pain-reporter is expressed in insulin-producing cells (IPCs) in the adult brain. IPC-specific knockdown of pain expression, ablation of IPCs, and suppression of neurosecretion from IPCs enhance female sexual receptivity. Considering that Pain is a cation channel with Ca2+ permeability, pain knockdown may disturb intracellular Ca2+ signaling in IPCs, leading to defects in the neurosecretion. Thus, we examined whether lack of Drosophila Insulin-like peptides affect female sexual receptivity. In Drosophila, Insulin-like peptide 2, 3 and 5 (Ilp2, Ilp3 and Ilp5) are co-expressed in the IPCs. Females homozygous for Ilp2-, Ilp3-, or Ilp5-knockout (KO) showed hyper sexual receptivity, and targeted expression of Ilp2 RNAi in IPCs phenocopied the phenotype of Ilp2-KO females. Thus, our results suggest that Pain regulates female sexual receptivity through Ilp-secretion.