N-methyl-d-aspartate receptor antagonism modulates P300 event-related potentials and associated activity in salience and central executive networks.

Autor: de la Salle S; School of Psychology, University of Ottawa, Ottawa, ON, Canada., Shah D; School of Psychology, University of Ottawa, Ottawa, ON, Canada., Choueiry J; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Bowers H; Department of Psychology, University of Guelph, Guelph, ON, Canada., McIntosh J; The Royal's Institute of Mental Health Research, Ottawa, ON, Canada., Carroll B; The Royal's Institute of Mental Health Research, Ottawa, ON, Canada., Ilivitsky V; Department of Psychiatry, University of Ottawa and the Royal Ottawa Mental Health Centre, Ottawa, ON, Canada., Knott V; School of Psychology, University of Ottawa, Ottawa, ON, Canada; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada; The Royal's Institute of Mental Health Research, Ottawa, ON, Canada; Department of Psychiatry, University of Ottawa and the Royal Ottawa Mental Health Centre, Ottawa, ON, Canada. Electronic address: Verner.Knott@theroyal.ca.
Jazyk: angličtina
Zdroj: Pharmacology, biochemistry, and behavior [Pharmacol Biochem Behav] 2021 Dec; Vol. 211, pp. 173287. Date of Electronic Publication: 2021 Oct 12.
DOI: 10.1016/j.pbb.2021.173287
Abstrakt: Impairments in auditory information processing in schizophrenia as indexed electrophysiologically by P300 deficits during novelty (P3a) and target (P3b) processing are linked to N -methyl- D -aspartate receptor (NMDAR) dysfunction. This study in 14 healthy volunteers examined the effects of a subanesthetic dose of the NMDAR antagonist ketamine on P300 and their relationship to psychomimetic symptoms and cortical source activity (with eLORETA). Ketamine reduced early (e- P3a) and late (l-P3a) novelty P300 at sensor (scalp)-level and at source-level in the salience network. Increases in dissociation symptoms were negatively correlated with ketamine-induced P3b changes, at sensor-level and source-level, in both salience and central executive networks. These P3a alterations during novelty processing, and the symptom-related P3b changes during target processing support a model of NMDAR hypofunction underlying disrupted auditory attention in schizophrenia.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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