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

被引:4
作者
de la Salle, Sara [1 ]
Shah, Dhrasti [1 ]
Choueiry, Joelle [2 ]
Bowers, Hayley [3 ]
McIntosh, Judy [4 ]
Carroll, Brooke [4 ]
Ilivitsky, Vadim [5 ,6 ]
Knott, Verner [1 ,2 ,4 ,5 ,6 ]
机构
[1] Univ Ottawa, Sch Psychol, Ottawa, ON, Canada
[2] Univ Ottawa, Dept Cellular & Mol Med, Ottawa, ON, Canada
[3] Univ Guelph, Dept Psychol, Guelph, ON, Canada
[4] Royals Inst Mental Hlth Res, Ottawa, ON, Canada
[5] Univ Ottawa, Dept Psychiat, Ottawa, ON, Canada
[6] Royal Ottawa Mental Hlth Ctr, Ottawa, ON, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Involuntary and voluntary attention; Event-related potentials; P300; P3a; P3b; Nmethyl-D-aspartate; Schizophrenia; LATE ERP RESPONSES; FUNCTIONAL CONNECTIVITY; MISMATCH NEGATIVITY; INTEGRATIVE THEORY; PREFRONTAL CORTEX; POSITIVE SYMPTOMS; SIMULTANEOUS EEG; DEFAULT-MODE; SCHIZOPHRENIA; BRAIN;
D O I
10.1016/j.pbb.2021.173287
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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.
引用
收藏
页数:12
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