| First Author | Westerink RH | Year | 2006 |
| Journal | J Neurochem | Volume | 99 |
| Issue | 2 | Pages | 628-40 |
| PubMed ID | 16824046 | Mgi Jnum | J:119287 |
| Mgi Id | MGI:3701719 | Doi | 10.1111/j.1471-4159.2006.04099.x |
| Citation | Westerink RH, et al. (2006) Dual role of calbindin-D28K in vesicular catecholamine release from mouse chromaffin cells. J Neurochem 99(2):628-40 |
| abstractText | 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. |
