4.7 Article

Synapsins as mediators of BDNF-enhanced neurotransmitter release

Journal

NATURE NEUROSCIENCE
Volume 3, Issue 4, Pages 323-329

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/73888

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Funding

  1. NIA NIH HHS [AG15072] Funding Source: Medline
  2. NIMH NIH HHS [MH39327] Funding Source: Medline

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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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