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Pharmacological research

ISSN 1096-1186

9 papers in the library · 108 citations · publishing 2023-2026

Papers

IUPHAR - invited review - Ibogaine - A legacy within the current renaissance of psychedelic therapy.

Pharmacological research April 1, 2023 Deborah C. Mash 37 citations

Ibogaine is a psychoactive substance that alters perception and mood and can interrupt addictive behaviors. It has a long history of ethnobotanical use in low doses for combating fatigue, hunger, and thirst, and in high doses as a sacrament in African rituals. In the 1960s, self-help groups reported that a single dose alleviated drug craving, opioid withdrawal, and prevented relapse for weeks to years. Ibogaine is rapidly metabolized to noribogaine, and both interact with multiple central nervous system targets, showing predictive validity in animal addiction models. Over ten thousand people have sought unregulated treatment, and open-label pilot studies show positive benefit. Ibogaine has regulatory approval for a Phase 1/2a clinical trial.

Novel rapid treatment options for adolescent depression.

Pharmacological research March 1, 2024 Sandra Ledesma-Corvi, Jordi Jornet-Plaza, Laura Gálvez-melero et al. 22 citations

Adolescent depression often requires faster-acting treatments than standard selective serotonin reuptake inhibitors, which take weeks to work. This review examines promising fast-acting options for adolescents, including non-pharmacological neuromodulation (electroconvulsive therapy and other brain stimulation) and pharmacological approaches such as ketamine, classical psychedelics, and cannabidiol. Most clinical evidence for these therapies comes from adult studies, but recent preclinical work is beginning to address sex-, age-, and dose-related differences that may affect efficacy and safety in adolescents. The authors call for more clinical studies and for designing novel treatments that are both safe and fast-acting for this age group.

Mind over matter: the microbial mindscapes of psychedelics and the gut-brain axis.

Pharmacological research September 1, 2024 Giorgia Caspani, Simon G D Ruffell, WaiFung Tsang et al. 13 citations

Psychedelics show promise for treating psychiatric disorders, but current explanations focus mainly on their action at serotonin receptors in the brain. This review argues that the gut microbiota, via the gut-brain axis, may also play a role. Evidence suggests psychedelics can alter gut microbiota composition, and microbial metabolism might influence psychedelic effects. The authors call for incorporating microbiome hypotheses into future research, which could lead to personalized psychedelic therapies tailored to individual gut microbiota profiles.

IUPHAR-review: The integration of classic psychedelics into current substance use disorder treatment models.

Pharmacological research January 1, 2024 David B Yaden, Andrea P Berghella, Peter S Hendricks et al. 12 citations

Classic psychedelic-assisted therapies show initial promise for treating substance use disorders (SUDs) and may become legally available options. This article describes how these therapies could fit within current evidence-based SUD treatments, suggesting broad compatibility with most mainstream clinical approaches.

IUPHAR Article: Psilocybin induces long-lasting effects via 5-HT2A receptors in mouse models of chronic pain.

Pharmacological research May 1, 2025 Eda Koseli, Belle Buzzi, Torin Honaker et al. 11 citations

Psilocybin and a similar psychedelic, DOI, reduced pain-related behaviors in mice with chronic pain. In a mouse model of chemotherapy-induced nerve damage, both drugs reversed sensitivity to cold and touch in a dose-dependent manner, with different timing of effects. In a model of persistent inflammatory pain, they also reversed sensitivity to heat. These pain-relieving effects depended on activation of the 5-HT2A serotonin receptor. The findings suggest that classical psychedelics may be effective for treating chronic pain through this receptor pathway.

Modulation of the endocannabinoid system by (S)-ketamine in an animal model of depression.

Pharmacological research January 1, 2025 Nicole R Silva, Shokouh Arjmand, Luana B Domingos et al. 6 citations

In a rat model of depression (Flinders Sensitive Line), depressive behavior was negatively correlated with levels of the endocannabinoid 2-AG. A single dose of S-ketamine restored 2-AG levels and increased endocannabinoid signaling in the prefrontal cortex. Although S-ketamine decreased gene expression of the CB1 receptor and the enzyme FAAH, protein levels did not change significantly. S-ketamine increased CB1 receptor binding, and computer modeling suggested it may bind to CB1, CB2, GPR55, and FAAH. However, blocking CB1 receptors with rimonabant did not prevent S-ketamine's behavioral effects, indicating a complex interaction with the endocannabinoid system that requires further study.

Dynamic regulation of phosphorylation of NMDA receptor GluN2B subunit tyrosine residues mediates ketamine rapid antidepressant effects.

Pharmacological research July 1, 2024 Ke Wang, Xuan Tan, Kai-Mo Ding et al. 5 citations

Ketamine rapidly alleviates depression-like behaviors by restoring the balance of NR2B phosphorylation both inside and outside synapses in the medial prefrontal cortex. In mice subjected to chronic unpredictable stress, ketamine normalized abnormal levels of phosphorylated NR2B and the phosphatase STEP61 within one hour. The findings indicate that the rapid antidepressant effects of ketamine depend on dynamic regulation of NR2B phosphorylation, offering a new target for developing antidepressant treatments.

Muscarinic cannabinoid suppression of excitation, a novel form of coincidence detection.

Pharmacological research February 1, 2025 Michaela Dvorakova, Ken Mackie, Alex Straiker 2 citations

Coactivating muscarinic acetylcholine receptors and eliciting depolarization-induced suppression of excitation (DSE) in autaptic hippocampal neurons produces a roughly 40% inhibition of excitatory transmission lasting about 10 minutes. This inhibition, termed muscarinic cannabinoid suppression of excitation (MCSE), requires CB1 and muscarinic M3/M5 receptors and is absent in CB1 receptor knockout neurons. Once established, it is reversed by a CB1 antagonist but not a muscarinic antagonist, indicating persistent CB1 receptor activation. MCSE can be mimicked by coapplying muscarinic and cannabinoid agonists and depends on calcium release from internal stores. This represents a novel coincidence detection between cannabinoid and muscarinic signaling systems, potentially modulating hippocampal signaling with implications for learning, memory, epilepsy, and addiction.

Effect of intraoperative esketamine on moderate-to-severe depressive symptoms in major surgery patients: A randomized clinical trial.

Pharmacological research July 1, 2026 Yang Zhou, Wanchen Sun, Yuxuan Fu et al.

Among patients undergoing major surgery who had moderate-to-severe depressive symptoms before the operation, a single intraoperative dose of esketamine led to a higher rate of symptom remission three days after surgery compared with a placebo. In a randomized, double-blind trial of 435 patients, 28.3% in the esketamine group achieved remission versus 11.3% in the placebo group. Acute pain rates did not differ between groups. Esketamine treatment requires monitoring for possible dissociative side effects, and its clinical use for depressive symptoms should weigh benefits against risks.