当前位置: X-MOL 学术J. Psychiatr. Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Abnormal beta and gamma frequency neural oscillations mediate auditory sensory gating deficit in schizophrenia.
Journal of Psychiatric Research ( IF 4.8 ) Pub Date : 2020-02-01 , DOI: 10.1016/j.jpsychires.2020.01.014
Ann T Nguyen 1 , William P Hetrick 2 , Brian F O'Donnell 2 , Colleen A Brenner 1
Affiliation  

BACKGROUND Sensory gating is a process in which the brain's response to irrelevant and repetitive stimuli is inhibited. The sensory gating deficit in schizophrenia (SZ) is typically measured by the ratio or difference score of the P50 event-related potential (ERP) amplitudes in response to a paired click paradigm. While the P50 gating effect has usually been measured in relation to the peak amplitude of the S1 and S2 P50 ERPs, there is increasing evidence that inhibitory processes may be reflected by evoked or induced oscillatory activity during the inter-click interval in the beta (20-30 Hz) and gamma (30-50 Hz) frequency bands. We therefore examined the relationship between frequency specific activity in the inter-click interval with gating effects in the time and frequency domains. METHOD Paired-auditory stimuli were presented to 131 participants with schizophrenia and 196 healthy controls (HC). P50 ERP amplitudes to S1 and S2as well as averaged- and single-trial beta (20-30 Hz) and gamma (30-50 Hz) frequency power during the inter-click interval were measured from the CZ electrode site. RESULTS In the time domain, P50 gating deficits were apparent in both ratio and difference scores. This effect was mainly due to smaller S1 amplitudes in the patient group. SZ patients exhibited less evoked beta and gamma power, particularly at the 0-100 ms time point, in response to S1. Early (0-100 ms) evoked beta and gamma responses were critical in determining the S1 amplitude and extent of P50 gating across the delay interval for both HC and SZ. CONCLUSION Our findings support a disruption in initial sensory registration in those with SZ, and do not support an active mechanism throughout the delay interval. The degree of response to S1 and early beta and gamma frequency oscillations in the delay interval provides information about the mechanisms supporting auditory sensory gating, and may provide a framework for studying the mechanisms that support sensory inhibition.

中文翻译:

异常的β和γ频率神经振荡介导精神分裂症的听觉感觉门控缺陷。

背景技术感觉门控是其中大脑对无关的和重复的刺激的反应被抑制的过程。精神分裂症(SZ)的感觉门控缺陷通常是通过响应配对点击范例的P50事件相关电位(ERP)幅度的比率或差异评分来衡量的。虽然通常根据S1和S2 P50 ERP的峰值幅度来测量P50门控效应,但越来越多的证据表明,在beta的点击间隔内,诱发或诱发的振荡活动可能反映了抑制过程(20 -30 Hz)和伽玛(30-50 Hz)频段。因此,我们检查了点击间隔内的特定频率活动与时域和频域中的门控效应之间的关系。方法对131名精神分裂症患者和196名健康对照者进行听觉配对刺激。在点击间隔内,从CZ电极位置测量到S1和S2的P50 ERP振幅以及平均和单次测试的Beta(20-30 Hz)和γ(30-50 Hz)频率功率。结果在时域中,P50门控缺陷在比率和差异评分上均很明显。该效果主要是由于患者组中的S1振幅较小。SZ患者对S1的反应表现出较小的诱发β和γ诱发力,尤其是在0-100 ms时间点。早期(0-100 ms)诱发的β和γ响应对于确定HC和SZ的整个延迟间隔中S1振幅和P50门控的程度至关重要。结论我们的发现支持SZ患者最初的感觉配准中断,并不支持整个延迟间隔的主动机制。对S1以及延迟间隔中早期β和γ频率振荡的响应程度提供了有关支持听觉感觉门控的机制的信息,并且可以提供用于研究支持感觉抑制的机制的框架。
更新日期:2020-02-03
down
wechat
bug