ArticleBiological psychiatry2025
Ketamine Evokes Acute Behavioral Effects Via μ Opioid Receptor-Expressing Neurons of the Central Amygdala.
Article in Biological psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Is the antidepressant efficacy of ketamine and esketamine mediated via opioid mechanisms?European psychiatry : the journal of the Association of European Psychiatrists · 2026Pooled it
- Sex differences in placebo and antidepressant response to intranasal esketamine for treatment-resistant depression.Molecular psychiatry · 2026Article
- From identity to function: unveiling the cellular complexity of hypothalamic feeding circuits.Reviews in endocrine & metabolic disorders · 2026Review
- Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Antidepressants and the endogenous opioid system.Biochemical pharmacology · 2025Review
- Insights Into the Effects of Ketamine on the Opioid System.Biological psychiatry · 2025Article
- Ketamine-induced static and dynamic functional connectivity changes are modulated by opioid receptors and biological sex in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
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Abstract
backgroundKetamine has anesthetic, analgesic, and antidepressant properties, which may involve multiple neuromodulatory systems. In humans, the opioid receptor (OR) antagonist naltrexone blocks the antidepressant effect of ketamine. This mechanism may differentiate ketamine from other NMDA receptor antagonists. Animal models that reflect OR-dependent behavioral effects of ketamine may shed light on the brain regions and circuits that contribute to ketamine's antidepressant mechanism in humans.
methodsWe screened male and female wild-type mice for a behavioral response to ketamine that could be reversed by OR antagonists in several assays, including locomotor activation, analgesia, and the forced swim test. Whole-brain imaging of cFos expression in ketamine-treated mice, pretreated with naltrexone or vehicle, was used to identify brain areas that mediated ketamine/OR interactions. Region-specific pharmacological and genetic interference with μ OR (MOR) signaling was used to test predictions of whole-brain imaging results in a subset of behavioral assays.
resultsAmong a series of behavioral assays, only locomotor activation was sensitive to ketamine and blocked by an MOR-selective antagonist. Locomotor activation produced by the NMDA receptor antagonist MK-801 was not OR dependent. Whole-brain imaging revealed that cFos expression in neurons of the central amygdala (CeA) showed the greatest difference between ketamine in the presence versus absence of naltrexone. CeA neurons expressing both MOR and PKCδ were strongly activated by naltrexone, and selectively interrupting MOR function in the CeA either pharmacologically or genetically blocked the locomotor effects of ketamine.
conclusionsThese data suggest that ketamine acts at MORs expressed in CeA neurons to produce acute hyperlocomotion.
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