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谷氨酸能神经传递在失配负波(MMN)中的作用,MMN是一种听觉突触可塑性和变化检测的测量指标。

The Role of Glutamate Neurotransmission in Mismatch Negativity (MMN), A Measure of Auditory Synaptic Plasticity and Change-detection.

作者信息

Harms Lauren, Parras Gloria G, Michie Patricia T, Malmierca Manuel S

机构信息

School of Biomedical Sciences and Pharmacy, University of Newcastle, Australia; Hunter Medical Research Institute, University of Newcastle, Australia; Centre for Brain and Mental Health Research, University of Newcastle, Australia.

Cognitive and Auditory Neuroscience Laboratory, Institute of Neuroscience of León (INCYL), Salamanca, Spain; The Salamanca Institute for Biomedical Research (IBSAL), Salamanca, Spain.

出版信息

Neuroscience. 2021 Feb 21;456:106-113. doi: 10.1016/j.neuroscience.2020.01.046. Epub 2020 Feb 8.

Abstract

Mismatch negativity (MMN) is an electrophysiological signature that occurs in response to unexpected stimuli. It is often referred to as a measure of memory-based change detection, because the elicitation of a prediction error response relies on the formation of a prediction, which in turn, is dependent upon intact memory of previous auditory stimulation. As such, the MMN is altered in conditions in which memory is affected, such as Alzheimer's disease, schizophrenia and healthy aging. The most prominent pharmacological finding for MMN strengthens the link between MMN and synaptic plasticity, as glutamate N-methyl-d-aspartate receptor (NMDA-R) antagonists reduce the MMN response. However, recent data has begun to demonstrate that the link between NMDA-R function and MMN is not as clear as once thought, with low dose and low affinity NMDA-R antagonists observed to facilitate MMN.

摘要

失匹配负波(MMN)是一种电生理特征,它会在对意外刺激的反应中出现。它常被视为基于记忆的变化检测指标,因为预测误差反应的诱发依赖于预测的形成,而预测的形成又依赖于对先前听觉刺激的完整记忆。因此,在记忆受到影响的情况下,如阿尔茨海默病、精神分裂症和健康衰老过程中,MMN会发生改变。关于MMN最显著的药理学发现强化了MMN与突触可塑性之间的联系,因为谷氨酸N-甲基-D-天冬氨酸受体(NMDA-R)拮抗剂会降低MMN反应。然而,最近的数据开始表明,NMDA-R功能与MMN之间的联系并不像曾经认为的那么清晰,低剂量和低亲和力的NMDA-R拮抗剂被观察到会促进MMN。

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