| Literature DB >> 25796435 |
John D Graef1, Kimberly Newberry2, Amy Newton2, Rick Pieschl2, Eric Shields3, Fu-Ni Luan3, Jean Simmermacher3, David Luchetti4, Eric Schaeffer4, Yu-Wen Li2, Laszlo Kiss2, Linda J Bristow2.
Abstract
The long lasting antidepressant response seen following acute, i.v. ketamine administration in patients with treatment-resistant depression (TRD) is thought to result from enhanced synaptic plasticity in cortical and hippocampal circuits. Using extracellular field recordings in rat hippocampal slices, we show that a single dose of the non-selective NMDA receptor antagonist ketamine or CP-101,606, a selective antagonist of the NR2B subunit of the NMDA receptor, enhances hippocampal synaptic plasticity induced with high frequency stimulation (HFS) 24h after dosing - a time at which plasma concentrations of the drug are no longer detectable in the animal. These results indicate that acute inhibition of NMDA receptors containing the NR2B subunit can lead to long-lasting changes in hippocampal plasticity.Entities:
Keywords: Ex vivo; Hippocampus; Long-term potentiation; NMDA receptors; NR2B subunit; Plasticity; Treatment-resistant depression
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Year: 2015 PMID： 25796435 DOI： 10.1016/j.brainres.2015.03.019
Source DB: PubMed Journal: Brain Res ISSN： 0006-8993 Impact factor: 3.252