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Reduction of dopamine D2/3 receptor binding in the striatum after a single administration of esketamine, but not R-ketamine: a PET study in conscious monkeys

Kenji Hashimoto, Takeharu Kakiuchi, Hiroyuki Ohba, Shingo Nishiyama, Hideo Tsukada

European Archives of Psychiatry and Clinical Neuroscience April 18, 2016 DOI: 10.1007/s00406-016-0692-7 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Conscious monkeys
Interventions Esketamine R-ketamine
Dose 0.5 mg/kg
Duration Single infusion
Topics Ketamine Esketamine
Keywords Psychotomimetic Raclopride Dopamine receptor d2 Pharmacology Ventral striatum Nmda receptor Binding potential Anesthesia
Citations 125
Key findings Esketamine, but not R-ketamine, reduces dopamine D2/3 receptor binding availability in the striatum, suggesting esketamine-induced dopamine release that may relate to its psychotomimetic effects.

Abstract

R-ketamine appears to be a potent, long-lasting and safer antidepressant, relative to esketamine (S-ketamine), since it might be free of psychotomimetic side effects. Using [11C]raclopride and positron emission tomography (PET), we investigated whether esketamine and R-ketamine can affect dopamine D2/3 receptor binding in the conscious monkey brain. A single infusion of esketamine (0.5 mg/kg), but not R-ketamine (0.5 mg/kg), caused a reduction of binding availability of dopamine D2/3 receptor in the monkey striatum. This study suggests that unlike to R-ketamine, esketamine can cause dopamine release in the striatum, and that its release might be associated with psychotomimetic effects of esketamine.

In the evidence

This study is part of the evidence base for a synthesis in the library. Here is how each one recorded it.

  • Esketamine, but not R-ketamine, reduced dopamine D2/3 receptor binding availability in the striatum, suggesting dopamine release that may relate to psychotomimetic effects.

    Synthesized

Comparable studies

Other preclinical and animal studies on esketamine, most cited first.

Study Year Design Participants
Esketamine Prevents Postoperative Emotional and Cognitive Dysfunction by Suppressing Microglial M1 Polarization and Regulating the BDNF-TrkB Pathway in Ageing Rats with Preoperative Sleep Disturbance Aged mice 2024 Animal study
S-Ketamine Rapidly Reverses Synaptic and Vascular Deficits of Hippocampus in Genetic Animal Model of Depression Flinders Sensitive Line and Flinders Resistant Line rats 2016 Preclinical experimental study in a genetic rat model
Low-dose S-ketamine exerts antidepressant-like effects via enhanced hippocampal synaptic plasticity in postpartum depression rats. Rat model of postpartum depression induced by reproductive hormone withdrawal 2022 Animal study
Antidepressant effects of esketamine via the BDNF/AKT/mTOR pathway in mice with postpartum depression and their offspring. Mice with postpartum depression and their offspring 2024 Animal study
Electroconvulsive therapy combined with esketamine improved depression through PI3K/AKT/GLT-1 pathway. Human patients with severe depression and a rat model of depression 2025 Randomized controlled trial and animal study n = 12

Citations in the library

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