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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 via OpenAlex

Summary

AI-generated from the abstract

Esketamine, but not R-ketamine, reduces dopamine D2/3 receptor binding availability in the monkey striatum, indicating that esketamine triggers dopamine release in this brain region. This dopamine release may underlie the psychotomimetic side effects of esketamine. R-ketamine, in contrast, does not affect striatal dopamine D2/3 binding, consistent with its proposed safer profile as a rapid antidepressant. The findings suggest a neurochemical difference between the two ketamine enantiomers that could explain their distinct side-effect profiles.

Study at a glance

Characteristics Experimental study Peer reviewed
Population Conscious monkeys
Interventions Esketamine R-ketamine
Dose 0.5 mg/kg
Duration Single infusion
Topics Ketamine
Keywords Psychotomimetic Raclopride Dopamine receptor d2 Pharmacology
Citations 125
Key finding 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.

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