Dual role of calbindin‐D_28K in vesicular catecholamine release from mouse chromaffin cells

Abstract

Calbindin-D 28K is suggested to play a postsynaptic role in neurotransmission and in the regulation of the intracellular Ca 2+ concentration. However, it is still unclear whether calbindin-D 28K has a role in the regulation of exocytosis, either as Ca 2+ buffer or as Ca 2+ sensor. Amperometric recordings of catecholamine exocytosis from wild-type and calbindin-D 28K 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, Ca 2+ current recordings and Ca 2+ imaging experiments, including video-rate confocal laser scanning microscopy, revealed that the intracellular Ca 2+ dynamics are remarkably similar in wild-type and knockout cells. The combined results demonstrate that calbindin-D 28K 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 Ca 2+ buffer but also as a modulator of vesicular catecholamine release is discussed.

Amphetamine reduces vesicular dopamine content in dexamethasone‐differentiated PC12 cells only following l‐DOPA exposure

“…Mice were housed with food and water available ad libitum . Isolation of the adrenal glands was performed as described previously (Westerink et al. 2006).…”

Neonatal Exposure to Brominated Flame Retardant BDE-47 Reduces Long-Term Potentiation and Postsynaptic Protein Levels in Mouse Hippocampus

“…Chromaffin cells from mice exposed to vehicle or 68 mg (140 μmol)/kg bw BDE-47 were isolated and cultured as described previously (Westerink et al 2006). …”

Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?

“…In addition to its calcium-buffering properties, calbindin-D28k undergoes a conformational change on binding Ca 2ϩ and functions as a Ca 2ϩ sensor (120,121). It is required for normal signaling of synaptically evoked calcium transients (122) and is involved in synaptic plasticity (123), long-term potentiation (LTP) (124), and memory formation (125,126), and possibly in the regulation of exocytosis (synaptic secretion of neurotransmitters) (127). Also, in Purkinje cells in the cerebellum, calbindin-D28k appears to be directly involved in motor control (122,128), which could suggest a possible mechanism explaining motor deficits observed in vitamin D-deficient rats (see below).…”