title: 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.
authors: Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.
authors: Isabella
authors: I
authors: Ferando
authors: Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.
authors: Guido C
authors: GC
authors: Faas
authors: Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.|Department of Physiology, The David Geffen School of Medicine, University of California, Los Angeles, California, USA.
authors: Istvan
authors: I
authors: Mody
mesh_terms: D000818:Animals; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology*; D006624:Hippocampus / Q000378:metabolism*; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology*; D011963:Receptors, GABA-A / Q000378:metabolism; D027981:Symporters / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism*; D000096922:K Cl- Cotransporters
chemical_list: D011963:Receptors, GABA-A; D027981:Symporters; D000096922:K Cl- Cotransporters