| First Author | Ferando I | Year | 2016 |
| Journal | Nat Neurosci | Volume | 19 |
| Issue | 9 | Pages | 1197-200 |
| PubMed ID | 27500406 | Mgi Jnum | J:238236 |
| Mgi Id | MGI:5818636 | Doi | 10.1038/nn.4357 |
| Citation | Ferando I, et al. (2016) Diminished KCC2 confounds synapse specificity of LTP during senescence. Nat Neurosci 19(9):1197-200 |
| abstractText | 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. |
