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Michael Michaelides

Biobehavioral Imaging and Molecular Neuropsychopharmacology Section, National Institute on Drug Abuse Intramural Research Program, Baltimore, MD, USA.

3 papers in the library · 65 citations · publishing 2022-2025

Papers

Redefining Ketamine Pharmacology for Antidepressant Action: Synergistic NMDA and Opioid Receptor Interactions?

The American journal of psychiatry March 1, 2025 Marjorie R Levinstein, Reece C Budinich, Jordi Bonaventura et al. 49 citations

Ketamine, a racemic compound used as an anesthetic, analgesic, and recreational drug, is being investigated for treating refractory depression and comorbid conditions like anxiety, obsessive-compulsive disorder, and opioid use disorder. Although ketamine is traditionally classified as an NMDA receptor antagonist, this review argues its pharmacology should be redefined to include opioid receptors and the endogenous opioid system. The authors propose that ketamine's antidepressant effects may arise from bifunctional, synergistic interactions involving both NMDA and opioid receptors.

The dopaminergic effects of esketamine are mediated by a dual mechanism involving glutamate and opioid receptors.

Molecular psychiatry February 19, 2025 Arianna Rizzo, Maria Zelai Garçon-Poca, Amelie Essmann et al. 14 citations

Esketamine, a new antidepressant, works through a complex interaction with brain chemicals rather than a single target. In mice, esketamine increased movement and raised overall dopamine levels by slowing dopamine removal, not by boosting its release. It also reduced glutamate activity. However, it decreased spontaneous dopamine release events and blunted reward-triggered dopamine release, which lowered the mice's motivation to work for rewards. Some of these dopamine effects were partially blocked by naloxone, an opioid blocker, and depended on glutamate input. The findings suggest esketamine's effects on brain chemistry vary by brain circuit and behavioral state.

Sex dependence of opioid-mediated responses to subanesthetic ketamine

bioRxiv Preprint Server September 6, 2022 Tommaso Di Ianni, Matine M. Azadian, Sedona N. Ewbank et al. 2 citations preprint

Ketamine rapidly reduces depressive symptoms in treatment-resistant depression, but its mechanisms are not fully understood. Recent clinical evidence controversially suggests that ketamine's efficacy may depend on opioid signaling. In rats, blocking opioid receptors suppressed ketamine-induced neurophysiologic changes in brain regions linked to depression and reward, but did not affect changes from a more selective NMDA receptor antagonist. This opioid-dependent response was strongly sex-dependent: absent in females and reversed by removing male gonads. Similar sex-dependent opioid effects appeared in ketamine-evoked structural plasticity and behavioral sensitization. These results indicate that ketamine may induce affective responses via opioid signaling, with subject sex as a strong influence, warranting direct assessment in future clinical trials.