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Neurochemical Effects of Oxytocin in People at Clinical High Risk for Psychosis

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)601-615
Number of pages15
JournalEuropean Neuropsychopharmacology
Volume29
Issue number5
Early online date28 Mar 2019
DOIs
Publication statusPublished - 1 May 2019

King's Authors

Abstract

Alterations in neurochemical metabolites are thought to play a role in the pathophysiology of psychosis onset. Oxytocin, a neuropeptide with prosocial and anxiolytic properties, modulates glutamate neurotransmission in preclinical models but its neurochemical effects in people at high risk for psychosis are unknown. We used proton magnetic resonance spectroscopy (1H-MRS) to examine the effects of intranasal oxytocin on glutamate and other metabolites in people at Clinical High Risk for Psychosis (CHR-P) in a double-blind, placebo-controlled, crossover design. 30 CHR-P males were studied on two occasions, once after 40IU intranasal oxytocin and once after placebo. The effects of oxytocin on the concentration of glutamate, glutamate+glutamine and other metabolites (choline, N-acetylaspartate, myo-inositol) scaled to creatine were examined in the left thalamus, anterior cingulate cortex (ACC) and left hippocampus, starting approximately 75, 84 and 93 minutes post-dosing, respectively. Relative to placebo, administration of oxytocin was associated with an increase in choline levels in the ACC (p=.008, Cohen’s d =0.54). There were no other significant effects on metabolite concentrations (all p>.05). Our findings suggest that, at ~75-93 minutes post-dosing, a single dose of intranasal oxytocin does not alter levels of neurochemical metabolites in the thalamus, ACC, or hippocampus in those at CHR-P, aside from potential effects on choline in the ACC.

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