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Diminished KCC2 confounds synapse specificity of LTP during senescence.

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.

SUBMITTER: Ferando I

PROVIDER: S-EPMC5003660 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

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Diminished KCC2 confounds synapse specificity of LTP during senescence.

Ferando Isabella I Faas Guido C GC Mody Istvan I

Nature neuroscience 20160808 9

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 informatio ...[more]

PMID: 27500406

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