Abstract
Short-term monocular deprivation (STMD, patching one eye for 1-3 hours) disrupts interocular balance in adult humans, as measured psychophysically, and also in our present studies using anesthetized adult macaques, as measured with intrinsic signal optical imaging of the V1 ocular dominance columns. Surprisingly, in all these studies, the relative contribution of the patched eye was elevated after patch removal. V1 imaging studies using pattern deprivation rather than full occlusion STMD also yielded a similar rapid shift in interocular balance in which the contribution of the non-deprived eye showed a steady decrease during the deprivation of the other eye. Once the deprivation period ended, the non-deprived eye dramatically strengthened, despite the stimulus to this eye remaining constant during the entire experiment. Further experiments have shown that this STMD effect is not orientation-specific. To further probe the underlying mechanisms of the STMD effect, we tested "P-channel deprivation". As with the pattern deprivation studies, the stimuli were dichoptically viewed 4 degree gratings of various orientations. However during the 1-3hr deprivation period, one eye was presented with low contrast (8%), low spatial frequency (0.5c/deg) stimuli designed to only stimulate the magnocellular (M) pathways. The imaging data collected showed a shift in interocular balance to this "P-channel" STMD similar to that seen with pattern deprivation. These results suggest that the underlying neural mechanisms mediating STMD-induced shifts in interocular balance are binocular and unlikely to be magno-dominated (and also not orientation specific), but rather depends appreciably on parvo-channel activity. The weakened response for the non-deprived eye during the deprivation period is striking. It cannot be explained by adaptation or fatigue in the eye or cortex. These results suggests a dynamic mechanism for regulating interocular balance and gain that includes the neurons in V1.
Meeting abstract presented at VSS 2016