Kam Ka Yee, Chang Dorita H F
Department of Psychology, The University of Hong Kong, Hong Kong, China.
The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong, China.
Imaging Neurosci (Camb). 2024 Jul 22;2. doi: 10.1162/imag_a_00237. eCollection 2024.
Sensory eye dominance (SED) refers to a functional asymmetry of the two eyes that is thought to result from the visual cortex assigning uneven weighting to the two eyes' data. Dichoptic perceptual training has been shown to improve (reduce) SED in visually normal individuals, with behavioral improvements accompanied by alterations of neural responses in the primary visual cortex. The mechanisms underlying these learning-driven neural changes are not well understood. Here, using magnetic resonance spectroscopy, we determined how inhibitory mechanisms in the early visual cortex (EVC) govern SED plasticity by measuring γ-aminobutyric acid (GABA) concentration changes before and after perceptual training. Fifty normal-sighted observers were trained on a dichoptic or binocular variant of a signal-in-noise (left-right) motion discrimination task. We observed significant shifts in SED following dichoptic (but not binocular) training. Before training, both groups exhibited lower GABA concentrations in the EVC when signals were presented to the dominant eye. Only after dichoptic training, GABA concentrations in the EVC increased during presentations of signals to the dominant eye and decreased during presentations of signals to the non-dominant eye. Our data suggest that dichoptic training drives changes in SED by promoting a rebalancing of interocular inhibition in the EVC.
感觉性眼优势(SED)是指双眼的一种功能不对称,被认为是由于视觉皮层对双眼数据赋予不均衡权重所致。已证明双眼分视知觉训练可改善(降低)视力正常个体的SED,行为改善伴随着初级视觉皮层神经反应的改变。这些由学习驱动的神经变化背后的机制尚不清楚。在此,我们使用磁共振波谱技术,通过测量知觉训练前后γ-氨基丁酸(GABA)浓度变化,来确定早期视觉皮层(EVC)中的抑制机制如何控制SED可塑性。五十名视力正常的观察者接受了噪声中信号(左右)运动辨别任务的双眼分视或双眼变体训练。我们观察到双眼分视(而非双眼)训练后SED有显著变化。训练前,当信号呈现给优势眼时,两组在EVC中的GABA浓度均较低。仅在双眼分视训练后,当信号呈现给优势眼时,EVC中的GABA浓度增加,而当信号呈现给非优势眼时,GABA浓度降低。我们的数据表明,双眼分视训练通过促进EVC中眼间抑制的重新平衡来驱动SED变化。