期刊
NATURE NEUROSCIENCE
卷 3, 期 4, 页码 323-329出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/73888
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资金
- NIA NIH HHS [AG15072] Funding Source: Medline
- NIMH NIH HHS [MH39327] Funding Source: Medline
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.
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