Short-term synaptic plasticity is altered in mice lacking synapsin I

Cell. 1993 Nov 19;75(4):661-70. doi: 10.1016/0092-8674(93)90487-b.


Synapsin I, the major phosphoprotein of synaptic vesicles, is thought to play a central role in neurotransmitter release. Here we introduce a null mutation into the murine synapsin I gene by homologous recombination. Mice with no detectable synapsin I manifest no apparent changes in well-being or gross nervous system function. Thus, synapsin I is not essential for neurotransmitter release. Electrophysiology reveals that mice lacking synapsin I exhibit a selective increase in paired pulse facilitation, with no major alterations in other synaptic parameters such as long-term potentiation. In addition to potential redundant functions shared with other proteins, synapsin I in normal mice may function to limit increases in neurotransmitter release elicited by residual Ca2+ after an initial stimulus.

Publication types

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

MeSH terms

  • Animals
  • Base Sequence
  • Catecholamines / physiology
  • Genes
  • Hippocampus / physiology
  • In Vitro Techniques
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Neuronal Plasticity*
  • Neurotransmitter Agents / metabolism
  • Oligodeoxyribonucleotides / chemistry
  • Restriction Mapping
  • Synapsins / physiology*
  • Synaptic Transmission
  • Time Factors


  • Catecholamines
  • Neurotransmitter Agents
  • Oligodeoxyribonucleotides
  • Synapsins