Processing deficits in primary visual cortex of amblyopic cats.

Early esotropic squint frequently results in permanent visual deficits in one eye, referred to as strabismic amblyopia. The neurophysiological substrate corresponding to these deficits is still a matter of investigation. Electrophysiological evidence is available for disturbed neuronal interactions in both V1 and higher cortical areas. In this study, we investigated the modulation of responses in cat V1 to gratings at different orientations and spatial frequencies (SFs; 0.1-2.0 cycles/degrees) with optical imaging of intrinsic signals. Maps evoked by both eyes were well modulated at most spatial frequencies. The layout of the maps resembled that of normal cats, and iso-orientation domains tended to cross adjacent ocular dominance borders preferentially at right angles. Visually evoked potentials (VEPs) were recorded at SFs ranging from 0.1 to 3.5 cycles/degrees and revealed a consistently weaker eye for the majority of squinting cats. At each SF, interocular differences in VEP amplitudes corresponded well with differences in orientation response and selectivity in the maps. At 0.7-1.3 cycles/ degrees, population orientation selectivity was significantly lower for the weaker eye in cats with VEP differences compared with those with no VEP amplitude differences. In addition, the cutoff SF, above which gratings no longer induced orientation maps, was lower for the weaker eye (> or =1.0 cycles/degrees). These data reveal a close correlation between the loss of visual acuity in amblyopia as assessed by VEPs and the modulation of neuronal activation as seen by optical imaging of intrinsic signals. Furthermore, the results indicate that amblyopia is associated with altered intracortical processing already in V1.