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Consistent with this, we previously showed in nucleus accumbens (NA<\/jats:styled-content>c) medium spiny neurons (MSN<\/jats:styled-content>s) that reduced mGlu1 tone enables and mGlu1 positive allosteric modulation reverses the elevation of CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content> levels in the NA<\/jats:styled-content>c that underlies enhanced cocaine craving in the \u201cincubation of craving\u201d rat model of addiction. To better understand mGlu1\/CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content> interactions, we used a NA<\/jats:styled-content>c\/prefrontal cortex co\u2010culture system in which NA<\/jats:styled-content>c MSN<\/jats:styled-content>s express high CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content> levels, providing an in\u00a0vitro model for NA<\/jats:styled-content>c MSN<\/jats:styled-content>s after the incubation of cocaine craving. The non\u2010specific group I orthosteric agonist dihydroxyphenylglycine (10\u00a0min) decreased cell surface GluA1 but not GluA2, indicating CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content> internalization. This was prevented by mGlu1 (LY<\/jats:styled-content>367385) or mGlu5 (MTEP<\/jats:styled-content>) blockade. However, a selective role for mGlu1 emerged in studies of long\u2010term antagonist treatment. Thus, LY<\/jats:styled-content>367385 (24\u00a0hr) increased surface GluA1 without affecting GluA2, whereas MTEP<\/jats:styled-content> (24\u00a0hr) had no effect. In hippocampal neurons, scaling up of CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content>s can occur through a mechanism requiring retinoic acid (RA<\/jats:styled-content>) signaling and new GluA1 synthesis. Consistent with this, the LY<\/jats:styled-content>367385\u2010induced increase in surface GluA1 was blocked by anisomycin (translation inhibitor) or 4\u2010(diethylamino)\u2010benzaldehyde (RA<\/jats:styled-content> synthesis inhibitor). Thus, mGlu1 transmission tonically suppresses cell surface CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content> levels, and decreasing mGlu1 tone increases surface CP<\/jats:styled-content>\u2010AMPAR<\/jats:styled-content>s via RA<\/jats:styled-content> signaling and protein translation. These results identify a novel mechanism for homeostatic plasticity in NAc MSNs.<\/jats:p>","DOI":"10.1111\/ejn.14151","type":"journal-article","created":{"date-parts":[[2018,9,17]],"date-time":"2018-09-17T18:08:51Z","timestamp":1537207731000},"page":"2590-2601","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["mGlu1 tonically regulates levels of calcium\u2010permeable AMPA<\/scp> receptors in cultured nucleus accumbens neurons through retinoic acid signaling and protein translation"],"prefix":"10.1111","volume":"50","author":[{"given":"Jessica A.","family":"Loweth","sequence":"first","affiliation":[{"name":"Department of Neuroscience The Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy M.","family":"Reimers","sequence":"additional","affiliation":[{"name":"Department of Neuroscience The Chicago 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