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We demonstrated previously that acute stress produces identical spatial memory deficits in male and female mice but through distinct molecular mechanisms, with females exhibiting up\u2010regulation of N\u2010methyl\u2010D\u2010aspartate (NMDA) receptor subunits in the dorsal hippocampus (dHPC). Here, we tested whether pharmacological manipulation of NMDA receptors prevents stress\u2010induced memory deficits and hippocampal glutamatergic dysfunction in a sex\u2010dependent manner.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>Male and female mice were exposed to 2\u2009hours of restraint stress. We performed electrophysiological and molecular analysis of the glutamatergic synapse in the dHPC. We evaluated two non\u2010competitive NMDA receptor antagonists administered pre\u2010stress: MK\u2010801, which blocks synaptic and extrasynaptic NMDA receptors, and memantine, which preferentially blocks extrasynaptic NMDA receptors. We evaluated effects of both drugs on stress\u2010induced spatial memory impairment and the effect of memantine on hippocampal glutamatergic neurotransmission.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>Acute stress induces sex\u2010 and time\u2010dependent alterations in glutamate\u2013glutamine metabolism, with a striking increase in stressed females. This outcome was associated with female glutamatergic neurotransmission impairment, indicated by reduced miniature EPSC amplitude and AMPA\/NMDA ratio at CA3\u2013CA1 synapses. MK\u2010801 and memantine rescued stress\u2010induced spatial memory impairment in male and female mice, respectively. Memantine counteracted stress\u2010induced reduction in AMPA\/NMDA ratio in female mice, normalising synaptic strength at CA3\u2013CA1 synapses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>Acute stress disrupts hippocampal glutamatergic homeostasis through sex\u2010dependent pathophysiological mechanisms. The study of sex\u2010dependent mechanisms may lead to targeted pharmacological treatments for cognitive deficits in stress\u2010related disorders.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70500","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T03:35:53Z","timestamp":1779075353000},"page":"4939-4952","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Memantine prevents acute stress\u2010induced memory deficits by reversing sex\u2010dependent pathophysiological glutamatergic alterations in the dorsal hippocampus"],"prefix":"10.1111","volume":"183","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6920-439X","authenticated-orcid":false,"given":"Sebastiano A.","family":"Torrisi","sequence":"first","affiliation":[{"name":"Department of Biomedical and Biotechnological Sciences University of Catania  Catania Italy"},{"name":"Oasi Research Institute\u2010IRCCS Unit of Translational Neuropharmacology and Translational Neurosciences  Troina Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-1019-967X","authenticated-orcid":false,"given":"Lidia","family":"Diolos\u00e0","sequence":"additional","affiliation":[{"name":"Department of Biomedical and Biotechnological Sciences University of Catania  Catania Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7530-6835","authenticated-orcid":false,"given":"Giuseppe","family":"Aceto","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Universit\u00e0 Cattolica del Sacro Cuore  Rome Italy"},{"name":"Fondazione Policlinico Universitario A. 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