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Cell. 1993 Nov 19;75(4):661-70.

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

Author information

1
Department of Molecular Genetics, Howard Hughes Medical Institute, University of Texas Southwestern Medical School, Dallas 75235.

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.

PMID:
7902212
DOI:
10.1016/0092-8674(93)90487-b
[Indexed for MEDLINE]

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