Short-term synaptic plasticity is altered in mice lacking synapsin I.
Cell
; 75(4): 661-70, 1993 Nov 19.
Article
em En
| MEDLINE
| ID: mdl-7902212
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Sinapsinas
/
Plasticidade Neuronal
Limite:
Animals
Idioma:
En
Revista:
Cell
Ano de publicação:
1993
Tipo de documento:
Article