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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2002-7-8
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pubmed: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.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0953-816X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1976-82
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12099903-Amino Acid Sequence,
pubmed-meshheading:12099903-Animals,
pubmed-meshheading:12099903-Electric Stimulation,
pubmed-meshheading:12099903-Excitatory Amino Acid Antagonists,
pubmed-meshheading:12099903-Excitatory Postsynaptic Potentials,
pubmed-meshheading:12099903-GABA Antagonists,
pubmed-meshheading:12099903-GAP-43 Protein,
pubmed-meshheading:12099903-Gene Expression,
pubmed-meshheading:12099903-Hippocampus,
pubmed-meshheading:12099903-Long-Term Potentiation,
pubmed-meshheading:12099903-Mice,
pubmed-meshheading:12099903-Mice, Transgenic,
pubmed-meshheading:12099903-Neurons,
pubmed-meshheading:12099903-Organ Culture Techniques,
pubmed-meshheading:12099903-Phenotype,
pubmed-meshheading:12099903-Phorbol 12,13-Dibutyrate,
pubmed-meshheading:12099903-Phosphorylation,
pubmed-meshheading:12099903-Point Mutation,
pubmed-meshheading:12099903-Protein Kinase C,
pubmed-meshheading:12099903-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:12099903-Synaptic Transmission,
pubmed-meshheading:12099903-Up-Regulation
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pubmed:year |
2002
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pubmed:articleTitle |
A point mutant of GAP-43 induces enhanced short-term and long-term hippocampal plasticity.
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pubmed:affiliation |
Neuropharmacology, Centre Médical Universitaire, rue M. Servet 1, 1211 Geneva 4, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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