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                <term xml:lang="en">PROTEIN-KINASE-C</term>
                <term xml:lang="en">CALCIUM</term>
                <term xml:lang="en">INSECTE</term>
                <term xml:lang="en">IN-VITRO</term>
                <term xml:lang="en">CHLORIDE CHANNEL</term>
                <term xml:lang="en">OLFACTORY TRANSDUCTION</term>
                <term xml:lang="fr">ANTENNAL NEURONS</term>
                <term xml:lang="fr">SENSORY NEURONS</term>
                <term xml:lang="fr">CURRENTS</term>
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              <p>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 K-1/2 of 2.8 mu M. Intracellular and extracellular anionic and cationic substitutions demonstrated that Cl- carries this current. The anion permeability sequence I- &gt; NO3- &gt; Br- &gt; Cl- &gt; CH3SO(3)(-) &gt;&gt; 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.</p>
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