School of Psychology, University of Ottawa, Ottawa, ON, Canada.
Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Pharmacol Biochem Behav. 2021 Dec;211:173287. doi: 10.1016/j.pbb.2021.173287. Epub 2021 Oct 12.
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.
精神分裂症患者听觉信息处理受损，表现在新颖性（P3a）和目标（P3b）处理期间 P300 缺陷，与 N-甲基-D-天冬氨酸受体（NMDAR）功能障碍有关。这项对 14 名健康志愿者的研究，考察了亚麻醉剂量的 NMDAR 拮抗剂氯胺酮对 P300 的影响及其与拟精神病症状和皮质源活动的关系（采用 eLORETA）。氯胺酮降低了早期（e-P3a）和晚期（l-P3a）新颖性 P300，在传感器（头皮）水平和突显网络中的源水平。分离症状的增加与氯胺酮诱导的 P3b 变化呈负相关，在突显和中央执行网络中，在传感器水平和源水平上均如此。这些新颖性处理过程中的 P3a 改变，以及目标处理过程中与症状相关的 P3b 改变，支持了 NMDAR 功能低下导致精神分裂症听觉注意力障碍的模型。
