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Nat Neurosci. 2016 Sep;19(9):1197-200. doi: 10.1038/nn.4357. Epub 2016 Aug 8.

Diminished KCC2 confounds synapse specificity of LTP during senescence.

Author information

1
Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.
2
Department of Physiology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Abstract

The synapse specificity of long-term potentiation (LTP) ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months) mice, LTP was relayed to unstimulated synapses, blemishing its synapse specificity. Diminished levels of the K(+)/Cl(-) cotransporter KCC2 and a depolarizing GABAA receptor-mediated synaptic component following LTP were the most likely causes for the spreading of potentiation, unveiling mechanisms hindering information storage in the aged brain and identifying KCC2 as a potential target for intervention.

PMID:
27500406
PMCID:
PMC5003660
DOI:
10.1038/nn.4357
[Indexed for MEDLINE]
Free PMC Article

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