Abstract
Sensory eye dominance 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. Perceptual training protocols employing dichoptic presentation of signal-noise motion stimuli have been shown to improve sensory eye dominance in visually normal individuals. These behavioural changes are accompanied by alterations in neural responses in primary visual cortex and in training-feature-specific extrastriate visual cortex (the human motion complex). Here, using magnetic resonance spectroscopy, we sought to determine whether training-driven changes in sensory eye dominance are accompanied by changes in neurochemistry. Specifically, we measured changes in metabolic concentrations of γ-aminobutyric acid (GABA) in early visual cortex, before and after a five-day visual training protocol. Visually normal adults received perceptual training on a dichoptic or a control (binocular) signal-in-noise motion discrimination (left-right) task over five consecutive days (6000 trials). In the dichoptic variant, signal dots carrying a coherent motion direction and noise dots carrying random motion directions were presented to different eyes. In the binocular variant, signal and noise dots were presented to both eyes. Results showed that sensory eye dominance improved following dichoptic perceptual training only. Before training, we found clear interocular differences in the concentration of GABA. Specifically, GABA concentration in early visual cortex was lower when signals were presented to the dominant eye than when signals were presented to the non-dominant eye. Importantly, after dichoptic perceptual training, GABA concentrations in early visual cortex increased during presentations of signals to the dominant eye, such that they were comparable to GABA concentrations observed during presentations of signals to the non-dominant eye. Our data suggest that dichoptic training-driven changes in sensory eye dominance are potentially driven by a rebalancing of interocular inhibition in the primary visual areas.