Synapsins as mediators of BDNF-enhanced neurotransmitter release

Nat Neurosci. 2000 Apr;3(4):323-9. doi: 10.1038/73888.


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 a causal link of synapsin phosphorylation via BDNF, TrkB receptors and MAP kinase with downstream facilitation of neurotransmitter release.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Brain-Derived Neurotrophic Factor / pharmacology*
  • Enzyme Inhibitors / pharmacology
  • Flavonoids / pharmacology
  • Gene Expression Regulation, Enzymologic
  • Glutamic Acid / metabolism*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Neurons / enzymology
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Stimulation, Chemical
  • Synapsins / genetics
  • Synapsins / metabolism*
  • Synaptic Transmission / drug effects*
  • Synaptic Transmission / physiology*
  • Synaptosomes / enzymology


  • Brain-Derived Neurotrophic Factor
  • Enzyme Inhibitors
  • Flavonoids
  • Synapsins
  • Glutamic Acid
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one