N-methyl-d-aspartate receptor antagonism modulates P300 event-related potentials and associated activity in salience and central executive networks.
S. de la Salle, D. Shah, J. Choueiry, H. Bowers, J. McIntosh, Brooke Carroll, V. Ilivitsky, V. Knott
Pharmacology, Biochemistry and Behavior October 1, 2021 DOI: 10.1016/j.pbb.2021.173287 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study in healthy volunteers Peer reviewed |
|---|---|
| Sample size | 14 |
| Population | Healthy volunteers |
| Intervention | Ketamine |
| Dose | subanesthetic dose |
| Measures | P300 (P3a, P3b), eLORETA |
| Key findings | Ketamine reduced early and late novelty P300 (P3a) at sensor and source levels in the salience network. Increases in dissociation symptoms were negatively correlated with ketamine-induced P3b changes at sensor and source levels in the salience and central executive networks. The authors argue these findings support a model of NMDAR hypofunction underlying disrupted auditory attention in schizophrenia. |
Abstract
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.