Purpose
Short-term monocular deprivation (STMD, patching one eye for 2.5 hours) markedly alters interocular balance in adult humans, as measured psychophysically (Lunghi et al 2011; Zhou et al 2013). In those studies, the relative contribution of the patched eye was elevated for more than an hour after patch removal. Now using intrinsic optical imaging in anesthetized macaque primary visual cortex (V1), we sought a parallel impact of STMD on interocular balance as measured by the strength of the V1 ocular dominance columns (ODC). Single-unit recordings in V1 with STMD, explored the neural correlates of these changes interocular balance at the neuronal level.
Methods
Optical imaging of V1 provided an initial ODC map for the imaging studies, and to guide the placement of single-unit electrodes. After measuring the baseline monocular and binocular responses, one eye was "deprived" by viewing a mean gray screen while the other eye continued to view the same stimuli and imaging or electrophysiological recordings proceeded. This MD phase lasted 2 hours, then visual stimuli and imaging or recordings continued another 2 hours.
Results
The imaging data were analyzed for ODC maps and for ODC signal strength (fractional reflectance change). Single cell responses to monocular and binocular stimuli were plotted before, during and after STMD. During STMD, the imaging data showed a steady decrease in the non-deprived eye strength, which dramatically shifted course (increased) after STMD even though stimulus in this eye was unaltered. The single-unit recordings revealed several different types of cell responses, including cells that showed unremarkable shifts in responses due to the STMD, other cells that exhibited an apparent strengthening of the non-deprived eye during STMD, and cells where the non-deprived eye showed dramatic drops in responsivity during STMD, consistent with the observed imaging (and psychophysical) results.
Conclusions
The weakened response for the non-deprived eye during and immediately after patching was striking. It cannot be explained by adaptation in the eye or cortex. We have now also observed electrophysiologically a corresponding alteration of interocular balance at the single cell level. These results matches the previous psychophysical studies and suggests a dynamic mechanism for regulating interocular balance and gain, one that is likely cortical in origin.