Abstract
The response of insect olfactory receptor neurons (ORNs) to odorants involves the opening of Ca2+-permeable channels, generating an increase in intracellular Ca2+ concentration. Here, we studied the downstream effect of this Ca2+ rise in cultured ORNs of the moth Spodoptera littoralis. Intracellular dialysis of Ca2+ from the patch pipette in whole-cell patch-clamp configuration activated a conductance with a K1/2 of 2.8 μm. Intracellular and extracellular anionic and cationic substitutions demonstrated that Cl− carries this current. The anion permeability sequence I− > NO3− > Br− > Cl− > CH3SO3− ≫ gluconate− of the Ca2+-activated Cl− channel suggests a weak electrical field pore of the channel. The Ca2+-activated current partly inactivated over time and did not depend on protein kinase C (PKC) and CaMKII activity or on calmodulin. Application of Cl− channel blockers, flufenamic acid, 5-nitro-2-(3-phenylpropylamino) benzoic acid, or niflumic acid reversibly blocked the Ca2+-activated current. In addition, lowering Cl− concentration in the sensillar lymph bathing the ORN outer dendrites caused a significant delay in pheromone response termination in vivo. The present work identifies a new Cl− conductance activated by Ca2+ in insect ORNs presumably required for ORN repolarization.