from dTrpA1-mediated activation of DPMs were not due to neurotransmitter release from DPMs themselves, but instead were a secondary result of gap–junction coupled APL activation and neurotransmitter release. In order to distinguish between these possibilities, we coexpressed dTrpA1 and the temperature-sensitive Dynamin mutant, Shits, in DPM neurons. Since Shits protein and mRNA are unlikely to pass through gap junctions, DPMShits expression should prevent neurotransmitter release in a cell-autonomous manner from DPM, but not affect APL neurons.