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Boris D. Heifets

35 papers in the library · 1,510 citations · publishing 2016-2026

Papers

Opioids diminish the placebo antidepressant response: Observational post hoc findings from a randomized controlled ketamine trial.

Journal of Affective Disorders July 15, 2025 Theresa R. Lii, Josephine R. Flohr, Robin L. Okada et al. 1 citation

The endogenous opioid system may influence the placebo antidepressant response. A post hoc analysis of a randomized, placebo-controlled trial of intravenous ketamine in depressed patients undergoing routine surgery tested whether baseline opioid use affected antidepressant responses. The analysis found that baseline opioid use significantly reduced post-treatment depression severity in patients who received placebo, but not in those who received ketamine. This reduction was independent of baseline depression severity, pain intensity, and ethnicity. The findings, based on a small sample, require confirmation by prospective controlled studies. Opioid use at baseline attenuated the placebo antidepressant response independently of pain, while the antidepressant response was preserved in opioid users who received ketamine.

5-HT2C receptors in the nucleus accumbens constrain the rewarding effects of MDMA.

bioRxiv : the preprint server for biology October 22, 2024 Matthew B Pomrenze, Sam Vaillancourt, Juliana S Salgado et al. 1 citation preprint

MDMA releases both dopamine and serotonin in the brain's reward center, the nucleus accumbens, but its strong serotonin release limits dopamine release and abuse potential. Using conditional knockout mice and direct brain infusions, the authors show that MDMA's serotonin release, acting through the serotonin transporter and 5-HT2C receptors, reduces the drug's reinforcing effects and conditioned place preference, while its prosocial effects are mediated by separate mechanisms. This platform predicts that (R)-MDMA, a novel entactogen, will have prosocial effects and low abuse potential.

Opioid receptor expressing neurons of the central amygdala gate behavioral effects of ketamine in mice.

bioRxiv : the preprint server for biology March 6, 2024 Matthew B Pomrenze, Sam Vaillancourt, Pierre Llorach et al. 1 citation preprint

Ketamine's effects on movement in mice are blocked by the opioid receptor antagonist naltrexone, but its analgesic and antidepressant-like effects are not. Whole-brain imaging identified the central amygdala as the region most affected by naltrexone, where neurons expressing mu-opioid receptors and PKCδ were strongly activated by naltrexone but not by ketamine. Disrupting mu-opioid receptor function in the central amygdala, either with drugs or genetic techniques, blocked ketamine's locomotor effects. These results indicate that mu-opioid receptors in the central amygdala gate certain behavioral effects of ketamine without being direct targets of the drug.

R-MDDMA is a Safer Analogue of MDMA with Therapeutic Potential.

ACS Chemical Neuroscience May 6, 2026 Maxemiliano V. Vargas, Cassandra J. Hatzipantelis, Lee E. Dunlap et al.

A safer analogue of MDMA, called R-MDDMA, shows promise for treating PTSD and depression without the abuse potential of MDMA. Unlike MDMA, R-MDDMA does not activate 5-HT2B receptors, induce serotonin release, cause head-twitch responses, affect body temperature, or increase locomotion at therapeutic doses. However, it still promotes structural neuroplasticity in cortical neurons, facilitates fear extinction learning, and produces sustained antidepressant-like effects. These results suggest that R-MDDMA might be a safer MDMA analogue with similar therapeutic properties.

CNSC-36. PSILOCYBIN INDUCES SUSTAINED GLIOMA GROWTH THROUGH SEROTONERGIC AND TRKB PATHWAYS

Neuro-Oncology November 1, 2025 Richard Drexler, Belgin Yalçın, Rebecca Mancusi et al.

High-grade gliomas integrate into serotonergic circuits via dorsal and median raphe projections, which drive calcium-mediated proliferation. Psilocybin, a serotonergic psychedelic selective for 5-HT2A with activity at TrkB, significantly increased proliferation in glioblastoma and DMG xenografts after a single dose, with effects persisting for at least two weeks. Calcium transients in glioma cells appeared within 30 minutes and remained detectable for two weeks. Genetic knockout of 5-HT2A nearly abolished psilocybin-induced proliferation, while TrkB knockout partially reduced it. These findings indicate that psilocybin promotes sustained glioma growth primarily through 5-HT2A activation, with a modulatory role for TrkB, suggesting caution for clinical use in brain tumor patients.

General anesthesia dissociates discrete components of ketamine neurophysiology

medRxiv August 7, 2025 Ben Deverett, Duan Li, Theresa R. Lii et al. preprint

Ketamine produces dissociative, analgesic, and antidepressant effects, but it is unclear whether its underlying neurophysiological signatures can be separated. In this observational cohort study, 52 participants (healthy volunteers, elective surgery patients, and patients with depression) received a subanesthetic infusion of ketamine or placebo, with or without general anesthesia. When ketamine was given under general anesthesia, its characteristic low-frequency brain wave augmentation was absent, while high-frequency power modulation was preserved. This selective modulation suggests a method for investigating the distinct roles of high- and low-frequency neural activity in ketamine's behavioral effects.

Opioids Diminish the Placebo Antidepressant Response: A Post Hoc Analysis of a Randomized Controlled Ketamine Trial.

medRxiv : the preprint server for health sciences November 2, 2024 Theresa R. Lii, Josephine R. Flohr, Robin L. Okada et al. preprint

The placebo antidepressant response was weaker in depressed patients who were already taking opioid medications, independent of their pain levels. In a re-analysis of a randomized trial, patients on chronic opioid therapy who received a placebo showed depression scores 10 points higher on the Montgomery-Åsberg Depression Rating Scale (MADRS) across 1 to 14 days after treatment, indicating less improvement. When measured as percent change, opioid users experienced 38.4% less improvement than non-users. For patients who received ketamine, baseline opioid use did not significantly affect depression scores. Pain intensity did not predict depression outcomes, and the link between depression and pain was negligible. These results come from a small, unregistered post hoc analysis and require confirmation.

Dreaming during anaesthesia: a scoping review.

British Journal of Anaesthesia August 1, 2026 Pilleriin Sikka, Sherry Hu, Boris D. Heifets

Dreaming during anaesthesia is common and has been documented for over a century, but remains poorly understood. This review of 157 studies from 1921 to 2024 involving 87,866 participants found that dream recall rates vary widely, from 3% to 8% in large clinical trials to 40% to 80% in experimental settings. Ketamine and propofol are most consistently associated with recall. Dreams are predominantly pleasant and feature everyday autobiographical content. Dream recall is not linked to intraoperative awareness, challenging the idea that dreams indicate inadequate anaesthetic depth. Higher home dream recall, preoperative suggestion, and immediate post-emergence assessment increase recall rates. Unpleasant dreams reduce willingness to undergo the same anaesthetic again. The positive nature and suggestibility of anaesthesia dreams suggest potential therapeutic uses.

The psychoplastogen tabernanthalog induces neuroplasticity without proximate immediate early gene activation.

Nature Neuroscience September 1, 2025 Isak K Aarrestad, Lindsay P. Cameron, Ethan M Fenton et al.

Nonhallucinogenic psychoplastogens like tabernanthalog (TBG) promote cortical neuroplasticity through the same biochemical pathway as classic psychedelics—involving 5-HT2A, TrkB, mTOR, and AMPA receptor activation—but without inducing an immediate glutamate burst or immediate early gene activation. TBG-induced cortical spinogenesis is required for its sustained antidepressant-like behavioral effect in rodents. These findings clarify how certain psychoplastogens can produce neuroplasticity without hallucinogenic effects, challenging assumptions that glutamate burst and IEG activation are necessary for psychedelic-induced neuroplasticity.