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These include impairments in executive functions, learning, planning, and cognitive flexibility. We have previously shown that moderate prenatal alcohol exposure (PAE) significantly impairs reversal learning, a measure of flexibility mediated across species by different brain areas that include the orbital frontal cortex (OFC). Reversal learning is likewise impaired by genetic or pharmacological inactivation of GluN2B subunit\u2010containing N\u2010methyl\u2010D\u2010aspartate receptors (NMDARs). In the current study, we tested the hypothesis that moderate PAE persistently alters the number and function of GluN2B subunit\u2010containing NMDARs in OFC pyramidal neurons of adult mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used a rodent model of fetal alcohol spectrum disorders and left offspring undisturbed until adulthood. Using whole\u2010cell, patch\u2010clamp recordings, we assessed NMDAR function in slices from 90\u2010 to 100\u2010day\u2010old male and female PAE and control mice. Pharmacologically isolated NMDA receptor\u2010mediated evoked excitatory postsynaptic currents (NMDA\u2010eEPSCs) were recorded in the absence and presence of the GluN2B antagonist, Ro25\u20106981(1\u00a0\u00b5M). In a subset of littermates, we evaluated the level of GluN2B protein expression in the synaptic fraction using Western blotting technique.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Our results indicate that PAE females show significantly larger (~23%) NMDA\u2010eEPSC amplitudes than controls, while PAE induced a significant decrease (~17%) in NMDA\u2010eEPSC current density of pyramidal neurons recorded in slices from male mice. NMDA\u2010eEPSC decay time was not affected in PAE\u2010exposed mice from either sex. The contribution of GluN2B subunit\u2010containing NMDARs to the eEPSCs was not significantly altered by PAE. Moreover, there were no significant changes in protein expression in the synaptic fraction of either PAE males or females.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings suggest that low\u2010to\u2010moderate PAE modulates NMDAR function in pyramidal neurons in a sex\u2010specific manner, although we did not find evidence that the effect is mediated by dysfunction of synaptic GluN2B subunit\u2010containing NMDARs.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.14697","type":"journal-article","created":{"date-parts":[[2021,9,15]],"date-time":"2021-09-15T03:46:39Z","timestamp":1631677599000},"page":"1994-2005","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Sex\u2010specific effect of prenatal alcohol exposure on N\u2010methyl\u2010D\u2010aspartate receptor function in orbitofrontal cortex pyramidal neurons of mice"],"prefix":"10.1111","volume":"45","author":[{"given":"Valentina","family":"Licheri","sequence":"first","affiliation":[{"name":"Department of Neurosciences University of New Mexico School of Medicine Albuquerque New Mexico USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jayapriya","family":"Chandrasekaran","sequence":"additional","affiliation":[{"name":"Department of Neurosciences University of New Mexico School of Medicine Albuquerque New Mexico USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clark W.","family":"Bird","sequence":"additional","affiliation":[{"name":"Department of Neurosciences University of New Mexico School of Medicine Albuquerque New Mexico USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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