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.