Diminished KCC2 confounds synapse specificity of LTP during senescence

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

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.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Excitatory Postsynaptic Potentials / physiology*
  • Hippocampus / metabolism*
  • Humans
  • Long-Term Potentiation / physiology*
  • Receptors, GABA-A / metabolism
  • Symporters / metabolism*
  • Synapses / metabolism*

Substances

  • Receptors, GABA-A
  • Symporters
  • potassium-chloride symporters