N-甲基-D-天冬氨酸受体拮抗作用调节突显和中央执行网络中 P300 事件相关电位及其相关活动。
N-methyl-d-aspartate receptor antagonism modulates P300 event-related potentials and associated activity in salience and central executive networks.
机构信息
School of Psychology, University of Ottawa, Ottawa, ON, Canada.
Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
出版信息
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。
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