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

Thomas W. Rosahl, Martin Geppert, Diane Spillane, Joachim Herz, Robert E Hammer, Robert C. Malenka, Thomas C. Südhof

Research output: Contribution to journalArticle

265 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)661-670
Number of pages10
JournalCell
Volume75
Issue number4
DOIs
StatePublished - Nov 19 1993

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ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

Rosahl, T. W., Geppert, M., Spillane, D., Herz, J., Hammer, R. E., Malenka, R. C., & Südhof, T. C. (1993). Short-term synaptic plasticity is altered in mice lacking synapsin I. Cell, 75(4), 661-670. https://doi.org/10.1016/0092-8674(93)90487-B