| First Author | Rosahl TW | Year | 1993 |
| Journal | Cell | Volume | 75 |
| Issue | 4 | Pages | 661-70 |
| PubMed ID | 7902212 | Mgi Jnum | J:15701 |
| Mgi Id | MGI:63816 | Doi | 10.1016/0092-8674(93)90487-b |
| Citation | Rosahl TW, et al. (1993) Short-term synaptic plasticity is altered in mice lacking synapsin I. Cell 75(4):661-70 |
| abstractText | 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. |
