Synapsin II negatively regulates catecholamine release |
| |
Authors: | Melissa Villanueva Keith Thornley George J Augustine R Mark Wightman |
| |
Institution: | (1) Department of Chemistry, The University of North Carolina at Chapel Hill, Venable Hall, CB#3290, Chapel Hill, NC 27599, USA;(2) Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA |
| |
Abstract: | We have assessed the role of synapsins in catecholamine release by comparing the properties of exocytosis in adrenal chromaffin
cells from wild-type and synapsin triple knock-out (TKO) mice. Brief depolarizations led to a greater amount of catecholamine
release in chromaffin cells from TKO mice in comparison to chromaffin cells from wild-type mice. This increase in catecholamine
release was due to an increased number of exocytotic events, while the properties of individual quanta of released catecholamine
were unchanged. Barium ions produced similar amounts of catecholamine release from TKO and wild-type chromaffin cells, suggesting
that the reserve pool of chromaffin granules is unchanged following loss of synapsins. Because expression of synapsin IIa
in TKO chromaffin cells rescued the defect in depolarization-induced exocytosis, the TKO phenotype apparently results from
loss of synapsin IIa. We conclude that synapsin IIa serves as a negative regulator of catecholamine release and that this
protein influences exocytosis from a readily releasable pool of chromaffin granules. Further, because these defects in catecholamine
release are different from those observed for glutamate and GABA release in TKO mice, we conclude that the functions of synapsins
differ for vesicles containing different types of neurotransmitters. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|