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A perforated patch‐clamp study of calcium currents and exocytosis in chromaffin cells of wild‐type and α1A knockout mice

Simultaneous recordings of inward whole‐cell Ca2+ channel currents (ICa) and increments of capacitance as an indication of exocytosis (ΔCm), were performed in voltage‐clamped single adrenal chromaffin cells from wild‐type and α1A subunit deficient mice, using the perforated‐patch configuration of the patch‐clamp technique. Using protocol #1 (one single Ca2+ channel blocker per cell), to dissect the components of ICa, L channels contributed 43%, N channels 35% and P/Q channels 30% to the total ICa of wild‐type cells. Using protocol #2 (cumulative sequential addition of 3 µm nifedipine, 1 µmω‐conotoxin GVIA, and 1 µmω‐agatoxin IVA), L, N and P/Q channels contributed 40%, 34% and 14%, respectively, to ICa; an R component of around 11% remained. In wild‐type mice the changes of ΔCm paralleled those of ICa. In α1A deficient mice the L component of ICa rose to 53% while the P/Q disappeared; the N and R components were similar. In these mice, ΔCm associated to N and R channels did not vary; however, the P/Q component was abolished while the L component increased by 20%. In conclusion, exocytosis was proportional to the relative density of each Ca2+ channel subtype, L, N, P/Q, R. Ablation of the α1A gene led to a loss of P/Q channel current and to a compensatory increase of L channel‐associated secretion; however, this compensation was not sufficient to maintain the overall exocytotic response, that was diminished by 35% in α1A‐deficient mice. This may be due to altered Ca2+ homeostasis in these mice, as compared to wild mouse chromaffin cells.