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Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses
Using targeted mouse mutants and pharmacologic inhibition of αCaMKII, we demonstrate that the αCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, αCaMKII regulates the number o...
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| Autors principals: | , , , , , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
2007
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2804046/ https://ncbi.nlm.nih.gov/pubmed/17660813 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nn1946 |
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