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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...

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Detalles Bibliográficos
Autores principales: Ferando, Isabella, Faas, Guido, Mody, Istvan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2016
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
Descripción
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.