Dual role of calbindin-D28K in vesicular catecholamine release from mouse chromaffin cells

Abstract

Calbindin-D28K is suggested to play a postsynaptic role in neurotransmission and in the regulation of the intracellular Ca2+ concentration. However, it is still unclear whether calbindin-D28K has a role in the regulation of exocytosis, either as Ca2+ buffer or as Ca2+ sensor. Amperometric recordings of catecholamine exocytosis from wild-type and calbindin-D28K knockout mouse chromaffin cells reveal a strong reduction in the number of released vesicles, as well as in the amount of neurotransmitter released per fusion event in knockout cells. However, Ca2+ current recordings and Ca2+ imaging experiments, including video-rate confocal laser scanning microscopy, revealed that the intracellular Ca2+ dynamics are remarkably similar in wild-type and knockout cells. The combined results demonstrate that calbindin-D28K plays an important and dual role in exocytosis, affecting both release frequency and quantal size, apparently without strong effects on intracellular Ca 2+ dynamics. Consequently, the possibility that calbindin-D 28K functions not only as a Ca2+ buffer but also as a modulator of vesicular catecholamine release is discussed. © 2006 The Authors.