Long-term potentiation and long-term depression (LTD) of synaptic efficacy, two major forms of synaptic plasticity, are believed to underlie learning processes and memory storage. We have recently shown that acute stress, through corticosterone release and stimulation of glucocorticoid receptors (GRs), facilitates the LTD elicited by the group 1 metabotropic glutamate receptor (mGluR) agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) in hippocampal CA1 neurons. However, it is unknown whether sustained corticosterone release, per se, is also able to facilitate DHPG-elicited LTD in control (i.e. unstressed) conditions, and if so, whether it acts on local (i.e. hippocampal) or distant GRs. Here, we show that a brief application of 100 nM corticosterone to rat hippocampal slices lowers the threshold for DHPG-elicited LTD, an effect mimicked by the local application of the GR agonist dexamethasone. These results show that high corticosterone release facilitates hippocampal CA1 mGluR-dependent LTD, and does so through local GRs.