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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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

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.[1]

References

  1. Short-term synaptic plasticity is altered in mice lacking synapsin I. Rosahl, T.W., Geppert, M., Spillane, D., Herz, J., Hammer, R.E., Malenka, R.C., Südhof, T.C. Cell (1993) [Pubmed]
 
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