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The bed nucleus of the stria terminalis (BNST) and\n                      <jats:italic>Crh<\/jats:italic>\n                      + neurons in this region play a key role in chronic ethanol\u2010induced increases in volitional intake, hypothesized to be driven by emergent negative affective behaviors. Excitatory\n                      <jats:italic>N<\/jats:italic>\n                      \u2010methyl\u2010\n                      <jats:sc>d<\/jats:sc>\n                      \u2010aspartate receptors (NMDARs) are a major target of ethanol, and chronic ethanol exposure has been shown to regulate NMDAR function and expression. Specifically, GluN2D subunit\u2010containing NMDARs have emerged as a target of interest due to their limited distribution and potential roles in affective behavior.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Male and female mice underwent a home cage chronic drinking forced abstinence model (CDFA) to assess the impact of 1\u2009day or 2\u2009weeks of ethanol abstinence on BNST synaptic transmission and BNST\n                      <jats:italic>Grin<\/jats:italic>\n                      gene expression. Constitutive and conditional BNST GluN2D knockout mice were used to assess the impact of GluN2D deletion on continuous access ethanol intake as well as negative affect behaviors, using the open field, elevated zero maze, and forced swim tasks.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We report here that excitatory transmission undergoes time\u2010dependent upregulation in BNST\n                      <jats:italic>Crh<\/jats:italic>\n                      + cells. Further, knockdown of dorsal BNST (dBNST) GluN2D expression significantly decreases ethanol intake in female, but not male, mice. While BNST\n                      <jats:italic>Grin2b<\/jats:italic>\n                      expression was significantly increased in protracted abstinence following CDFA, no differences in\n                      <jats:italic>Grin2d<\/jats:italic>\n                      expression were observed in the dBNST or dBNST\n                      <jats:italic>Crh<\/jats:italic>\n                      + neurons. Finally, we find that deletion of GluN2D fails to alter negative affect in ethanol\u2010na\u00efve female mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These data suggest a role for BNST GluN2D\u2010containing NMDARs in ethanol drinking but not ethanol abstinence, highlighting sex differences and behavioral specificity. Overall, these data further suggest roles for BNST synaptic signaling in volitional ethanol intake that are partially independent of actions on affective behavior.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.15432","type":"journal-article","created":{"date-parts":[[2024,8,23]],"date-time":"2024-08-23T22:42:31Z","timestamp":1724452951000},"page":"1876-1891","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<scp>BNST G<\/scp>\n                    lu\n                    <scp>N<\/scp>\n                    2\n                    <scp>D<\/scp>\n                    \u2010containing\n                    <scp>NMDAR<\/scp>\n                    s contribute to ethanol intake but not negative affective behaviors in female mice"],"prefix":"10.1111","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3144-5163","authenticated-orcid":false,"given":"Marie A.","family":"Doyle","sequence":"first","affiliation":[{"name":"Department of Neurobiology UMass Chan Medical School  Worcester Massachusetts USA"},{"name":"Department of Molecular Physiology and Biophysics Vanderbilt University  Nashville Tennessee USA"},{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory J.","family":"Salimando","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biophysics Vanderbilt University  Nashville Tennessee USA"},{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan E.","family":"Altemus","sequence":"additional","affiliation":[{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin K.","family":"Badt","sequence":"additional","affiliation":[{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle N.","family":"Bedenbaugh","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biophysics Vanderbilt University  Nashville Tennessee USA"},{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander S.","family":"Vardy","sequence":"additional","affiliation":[{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle N.","family":"Adank","sequence":"additional","affiliation":[{"name":"Vanderbilt Center for Addiction Research Vanderbilt University  Nashville Tennessee 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