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Neurosci."],"abstract":"<jats:p>Ketamine is a powerful glutamatergic long-lasting antidepressant, efficient in intractable major depression. Whereas ketamine\u2019s immediate psychomimetic side-effects were linked to glutamate changes, proton MRS (<jats:sup>1<\/jats:sup>H-MRS) showed an association between the ratio of glutamate and glutamine and delayed antidepressant effect emerging \u223c2 h after ketamine administration. While most <jats:sup>1<\/jats:sup>H-MRS studies focused on anterior cingulate, recent functional MRI connectivity studies revealed an association between ketamine\u2019s antidepressant effect and disturbed connectivity patterns to the posterior cingulate cortex (PCC), and related PCC dysfunction to rumination and memory impairment involved in depressive pathophysiology. The current study utilized the state-of-the-art single-voxel 3T sLASER <jats:sup>1<\/jats:sup>H-MRS methodology optimized for reproducible measurements. Ketamine\u2019s effects on neurochemicals were assessed before and \u223c3 h after intravenous ketamine challenge in PCC. Concentrations of 11 neurochemicals, including glutamate (CRLB \u223c 4%) and glutamine (CRLB \u223c 13%), were reliably quantified with the LCModel in 12 healthy young men with between-session coefficients of variation (SD\/mean) &amp;lt;8%. Also, ratios of glutamate\/glutamine and glutamate\/aspartate were assessed as markers of synaptic function and activated glucose metabolism, respectively. Pairwise comparison of metabolite profiles at baseline and 193 \u00b1 4 min after ketamine challenge yielded no differences. Minimal detectable concentration differences estimated with <jats:italic>post hoc<\/jats:italic> power analysis (power = 80%, alpha = 0.05) were below 0.5 \u03bcmol\/g, namely 0.39 \u03bcmol\/g (\u223c4%) for glutamate, 0.28 \u03bcmol\/g (\u223c10%) for Gln, \u223c14% for glutamate\/glutamine and \u223c8% for glutamate\/aspartate. 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