Differential effects of depolarization on intracellular calcium concentration in wild type and dunce Drosophila neurons

Abstract

AbstractUtilizing Fura 2‐AM fluorescence photometry, intracellular calcium concentration ∥[Ca2+]i) was measured in wild type and dunce cleavage‐arrested Drosophila neurons under resting condition and in response to KCl induced depolarization. Following KCl application, peak [Ca2+]i was greater in dunce (424 ± 29 nM) than in wild type neurons (246 ± 21 nM). Half decay time was shorter in dunce (65 ± 5 sec) than in wild type neurons (84 ± 6 sec). In cadmium‐containing and in calcium‐free external solutions, KCl application did not lead to any changes in [Ca2+]i in wild type and dunce neurons. Thus, the source of increase in [Ca2+]i seems to be Ca2+ influx from outside. Treatment with nifedipine and nimodipine did not affect [Ca2+]i increase in response to KCl application. This indicates that both wild type and dunce neuronal Ca2+ channels are not sensitive to these dihydropyridines. Pretreatment of wild type neurons with dibutyryl cAMP for 1 hour, prior to depolarization by KCl, resulted in peak [Ca2+]i of 369 ± 27 nM which is similar to untreated dunce neurons. The present results suggest that cAMP is implicated in modulating Ca2+ channels leading to enhanced Ca2+ influx in dunce neurons. Calcium extrusion and/or calcium buffering systems are possibly enhanced in the dunce mutant compared to the wild type. This disturbance in homeostatis of cytosolic calcium concentration in dunce neurons may be implicated in defective learning and memory.