Synapsins as mediators of BDNF-enhanced neurotransmitter release

被引：470
作者：
Jovanovic, JN
Czernik, AJ
Fienberg, AA
Greengard, P
Sihra, TS
机构：
[1] UCL, Dept Pharmacol, London WC1E 6BT, England
[2] Rockefeller Univ, Mol & Cellular Neurosci Lab, New York, NY 10021 USA
来源：
NATURE NEUROSCIENCE | 2000年 / 3卷 / 04期
关键词：
D O I：
10.1038/73888
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
We examined enhancement of synaptic transmission by neurotrophins at the presynaptic level. In a synaptosomal preparation, brain-derived neurotrophic factor (BDNF) increased mitogen-activated protein (MAP) kinase-dependent synapsin I phosphorylation and acutely facilitated evoked glutamate release. PD98059, used to inhibit MAP kinase activity, markedly decreased synapsin I phosphorylation and concomitantly reduced neurotransmitter release. The stimulation of glutamate release by BDNF was strongly attenuated in mice lacking synapsin I and/or synapsin II. These results indicate at causal link of synapsin phosphorylation via BDNF, TrkB receptors and MAP kinase with downstream facilitation of neurotransmitter release.
引用
收藏
页码：323 / 329
页数：7
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