
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.
Symporters, Long-Term Potentiation, Excitatory Postsynaptic Potentials, Receptors, GABA-A, Hippocampus, Article, K Cl- Cotransporters, Synapses, Animals, Humans
Symporters, Long-Term Potentiation, Excitatory Postsynaptic Potentials, Receptors, GABA-A, Hippocampus, Article, K Cl- Cotransporters, Synapses, Animals, Humans
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