Abstract

Background

Accumulating research suggests that altered levels of neurochemical metabolites -such as glutamate- play a role in psychosis pathophysiology, are present prior to onset in people at Clinical High Risk (CHR-P) and predict clinical outcomes. Oxytocin, a neuropeptide with prosocial and anxiolytic properties, modulates glutamate neurotransmission in animals but its neurochemical effects in CHR-P individuals remain unknown. The present study examined the effects of intranasal oxytocin on glutamate and glutamate+glutamine (primary hypothesis) and other neurochemical metabolites (secondary hypothesis) in CHR-P individuals.

Methods

In a double-blind, placebo-controlled, crossover design, 30 CHR-P males underwent two MRI scans at 3 Tesla, once after 40IU intranasal oxytocin and once after matched placebo (one-week wash-out). Proton magnetic resonance spectroscopy (1H-MRS) was used to measure the effects of oxytocin on glutamate, glutamate+glutamine and other metabolite levels (choline, N-acetylaspartate, myo-inositol) scaled to creatine in the hippocampus, anterior cingulate cortex and thalamus.

Results

Data analysis is currently ongoing, and the results will be presented at the conference.

Discussion

These results will provide the first neurophysiological evidence for the potential effects of oxytocin on neurochemical metabolites in CHR-P individuals. Given the current lack of evidence for effective treatments in this patient group, continued efforts to find novel molecules with a relevant profile of effects remains a priority.

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