Temperature and functional plasticity of L-type Ca2+ channels in Drosophila.

The question of optimization of ion channel function to surrounding temperatures in poikilothermic organisms remains largely uninvestigated. Here, we addressed it by studying the temperature-dependence of L-type Ca2+ channels (LTCCs) in Drosophila larval muscles in the context of their modulation by protein kinase A (PKA). LTCC currents were recorded between 4 and 30°C. Different aspects of LTCC function reached maxima between 15 and 25°C: conductance, tail current amplitude, inactivation rate, and the level of basal up-regulation by PKA (26% at 21°C). Anomalous temperature-dependencies of LTCC conductance and kinetics were similar in control and in the presence of the PKA inhibitor H-89. Analysis of deactivation kinetics revealed excessive tail currents at lower temperatures (up to 15°C), indicative of voltage-dependent facilitation of LTCCs. Tail current magnitude gradually decreased with temperature from a maximum at 15°C until a nearly complete disappearance at 30°C. Elimination of excessive tail currents at higher temperatures coincided with unusual slowing of inactivation, suggesting disruption of the facilitation by rising temperature, possibly through depletion of the pool of contributing channels. Overall, these results suggest the presence of a physiological plasticity optimum of LTCC function in the temperature range of normal Drosophila development.