The neurochemistry of learning-driven sensory eye dominance plasticity

Abstract 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.