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The typical antidepressant fluoxetine is known to induce plasticity in the adult rodent visual cortex, as assessed by a shift in ocular dominance, a classical model of brain plasticity, and a similar effect has been described for ketamine and its metabolite 2\n                    <jats:italic>R<\/jats:italic>\n                    ,6\n                    <jats:italic>R<\/jats:italic>\n                    \u2010hydroxynorketamine (\n                    <jats:italic>R<\/jats:italic>\n                    ,\n                    <jats:italic>R<\/jats:italic>\n                    \u2010HNK). Here, we demonstrate that ketamine (at 3 or 20\u2009mg\/kg) and\n                    <jats:italic>R<\/jats:italic>\n                    ,\n                    <jats:italic>R<\/jats:italic>\n                    \u2010HNK facilitated the shift in ocular dominance in monocularly deprived mice, after three injections, throughout the 7\u2010day monocular deprivation regimen. Notably, the comparison between the treatments indicates a higher effect size of\n                    <jats:italic>R<\/jats:italic>\n                    ,\n                    <jats:italic>R<\/jats:italic>\n                    \u2010HNK compared with ketamine. Treatment with ketamine or\n                    <jats:italic>R<\/jats:italic>\n                    ,\n                    <jats:italic>R<\/jats:italic>\n                    \u2010HNK failed to influence the levels of perineuronal nets (PNNs) surrounding parvalbumin\u2010positive interneurons. However, we observed in vitro that both ketamine and\n                    <jats:italic>R<\/jats:italic>\n                    ,\n                    <jats:italic>R<\/jats:italic>\n                    \u2010HNK are able to disrupt the tropomyosin\u2010related kinase B (TRKB) interaction with the protein tyrosine phosphatase sigma (PTP\u03c3), which upon binding to PNNs dephosphorylates TRKB. These results support a model where diverse drugs promote the reinstatement of juvenile\u2010like plasticity by directly binding TRKB and releasing it from PTP\u03c3 regulation, without necessarily reducing PNNs deposits.\n                  <\/jats:p>","DOI":"10.1111\/ejn.15929","type":"journal-article","created":{"date-parts":[[2023,2,5]],"date-time":"2023-02-05T23:14:40Z","timestamp":1675638880000},"page":"940-950","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Ketamine and its metabolite 2\n                    <i>R<\/i>\n                    ,6\n                    <i>R<\/i>\n                    \u2010hydroxynorketamine promote ocular dominance plasticity and release tropomyosin\u2010related kinase B from inhibitory control without reducing perineuronal nets enwrapping parvalbumin 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