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Diminished KCC2 confounds synapse-specificity of LTP during senescence
Synapse-specificity of LTP ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months-old) mice LTP was relayed to unstimulated synapses blemishing its synapse-specificity. Diminished levels of the K(+)/Cl(–) cotransporter KCC2 and a d...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003660/ https://www.ncbi.nlm.nih.gov/pubmed/27500406 http://dx.doi.org/10.1038/nn.4357 |
Sumario: | Synapse-specificity of LTP ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months-old) mice LTP was relayed to unstimulated synapses blemishing its synapse-specificity. Diminished levels of the K(+)/Cl(–) cotransporter KCC2 and a depolarizing GABA(A) receptor-mediated synaptic component following LTP were the most likely causes for spreading the potentiation, unveiling novel mechanisms hindering information storage in the aged brain, and identifying KCC2 as a potential target for intervention. |
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