Octopamine signaling via OctαR is essential for a well-orchestrated climbing performance of adult Drosophila melanogaster.

The biogenic amine octopamine (OA) orchestrates many behavioural processes in insects. OA mediates its function by binding to OA receptors belonging to the G protein-coupled receptors superfamily. Despite the potential relevance of OA, our knowledge about the role of each octopaminergic receptor and how signalling through these receptors controls locomotion still limited. In this study, RNA interference (RNAi) was used to knockdown each OA receptor type in almost all Drosophila melanogaster tissues using a tubP-GAL4 driver to investigate the loss of which receptor affects the climbing ability of adult flies. The results demonstrated that although all octopaminergic receptors are involved in normal negative geotaxis but OctαR-deficient flies had impaired climbing ability more than those deficient in other OA receptors. Mutation in OA receptors coding genes develop weak climbing behaviour. Directing knockdown of octαR either in muscular system or nervous system or when more specifically restricted to motor and gravity sensing neurons result in similar impaired climbing phenotype, indicating that within Drosophila legs, OA through OctαR orchestrated the nervous system control and muscular tissue responses. OctαR-deficient adult males showed morphometric changes in the length and width of leg parts. Leg parts morphometric changes were also observed in Drosophila mutant in OctαR. Transmission electron microscopy revealed that the leg muscles OctαR-deficient flies have severe ultrastructural changes compared to those of control flies indicating the role played by OctαR signalling in normal muscular system development. The severe impairment in the climbing performance of OctαR-deficient flies correlates well with the completely distorted leg muscle ultrastructure in these flies. Taken together, we could conclude that OA via OctαR plays an important multifactorial role in controlling locomotor activity of Drosophila.