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弱视中视觉皮层γ-氨基丁酸与知觉抑制

Visual cortical γ-aminobutyric acid and perceptual suppression in amblyopia.

作者信息

Mukerji Arjun, Byrne Kelly N, Yang Eunice, Levi Dennis M, Silver Michael A

机构信息

Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, United States.

Henry H. Wheeler, Jr. Brain Imaging Center, University of California, Berkeley, Berkeley, CA, United States.

出版信息

Front Hum Neurosci. 2022 Sep 2;16:949395. doi: 10.3389/fnhum.2022.949395. eCollection 2022.

DOI:10.3389/fnhum.2022.949395
PMID:36118971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9479630/
Abstract

In amblyopia, abnormal visual experience during development leads to an enduring loss of visual acuity in adulthood. Physiological studies in animal models suggest that intracortical GABAergic inhibition may mediate visual deficits in amblyopia. To better understand the relationship between visual cortical γ-aminobutyric acid (GABA) and perceptual suppression in persons with amblyopia (PWA), we employed magnetic resonance spectroscopy (MRS) to quantify GABA levels in both PWA and normally-sighted persons (NSP). In the same individuals, we obtained psychophysical measures of perceptual suppression for a variety of ocular configurations. In PWA, we found a robust negative correlation between the depth of amblyopia (the difference in visual acuity between the amblyopic and non-amblyopic eyes) and GABA concentration that was specific to visual cortex and was not observed in a sensorimotor cortical control region. Moreover, lower levels of visual cortical GABA were associated with weaker perceptual suppression of the fellow eye by the amblyopic eye and stronger suppression of the amblyopic eye by the fellow eye. Taken together, our findings provide evidence that intracortical GABAergic inhibition is an important component of the pathology of human amblyopia and suggest possible therapeutic interventions to restore vision in the amblyopic eye through enhancement of visual cortical GABAergic signaling in PWA.

摘要

在弱视中,发育过程中的异常视觉体验会导致成年后视力的持久丧失。动物模型的生理学研究表明,皮质内GABA能抑制可能介导弱视中的视觉缺陷。为了更好地理解弱视患者(PWA)视觉皮质γ-氨基丁酸(GABA)与知觉抑制之间的关系,我们采用磁共振波谱(MRS)来量化PWA和视力正常者(NSP)的GABA水平。在同一组个体中,我们获得了多种眼部配置下知觉抑制的心理物理学测量结果。在PWA中,我们发现弱视程度(弱视眼与非弱视眼之间的视力差异)与GABA浓度之间存在强烈的负相关,这种相关性在视觉皮质中具有特异性,在感觉运动皮质控制区域未观察到。此外,较低水平的视觉皮质GABA与弱视眼对健眼的较弱知觉抑制以及健眼对弱视眼的较强抑制有关。综上所述,我们的研究结果提供了证据,表明皮质内GABA能抑制是人类弱视病理的重要组成部分,并提示了通过增强PWA视觉皮质GABA能信号来恢复弱视眼视力的可能治疗干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c6c/9479630/27a5901cd133/fnhum-16-949395-g011.jpg
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