| First Author | Hulo S | Year | 2002 |
| Journal | Eur J Neurosci | Volume | 15 |
| Issue | 12 | Pages | 1976-82 |
| PubMed ID | 12099903 | Mgi Jnum | J:128162 |
| Mgi Id | MGI:3766349 | Doi | 10.1046/j.1460-9568.2002.02026.x |
| Citation | Hulo S, et al. (2002) A point mutant of GAP-43 induces enhanced short-term and long-term hippocampal plasticity. Eur J Neurosci 15(12):1976-82 |
| abstractText | The growth-associated protein GAP-43 (or neuromodulin or B-50) plays a critical role during development in mechanisms of axonal growth and formation of synaptic networks. At later times, GAP-43 has also been implicated in the regulation of synaptic transmission and properties of plasticity such as long-term potentiation. In a molecular approach, we have analyzed transgenic mice overexpressing different mutated forms of GAP-43 or deficient in GAP-43 to investigate the role of the molecule in short-term and long-term plasticity. We report that overexpression of a mutated form of GAP-43 that mimics constitutively phosphorylated GAP-43 results in an enhancement of long-term potentiation in CA1 hippocampal slices. This effect is specific, because LTP was affected neither in transgenic mice overexpressing mutated forms of non-phosphorylatable GAP-43 nor in GAP-43 deficient mice. The increased LTP observed in transgenic mice expressing a constitutively phosphorylated GAP-43 was associated with an increased paired-pulse facilitation as well as an increased summation of responses during high frequency bursts. These results indicate that, while GAP-43 is not necessary for LTP induction, its phosphorylation may regulate presynaptic properties, thereby affecting synaptic plasticity and the induction of LTP. |
