Amblyopia is a developmental disorder of pattern vision. After surgical creation of esotropic strabismus in the first weeks of life or after wearing -10 diopter contact lenses in one eye to simulate anisometropia during the first months of life, macaques often develop amblyopia. We studied the response properties of visual cortex neurons in six amblyopic macaques; three monkeys were anisometropic, and three were strabismic. In all monkeys, cortical binocularity was reduced. In anisometropes, the amblyopic eye influenced a relatively small proportion of cortical neurons; in strabismics, the influence of the two eyes was more nearly equal. The severity of amblyopia was related to the relative strength of the input of the amblyopic eye to the cortex only for the more seriously affected amblyopes. Measurements of the spatial frequency tuning and contrast sensitivity of cortical neurons showed few differences between the eyes for the three less severe amblyopes (two strabismic and one anisometropic). In the three more severely affected animals (one strabismic and two anisometropic), the optimal spatial frequency and spatial resolution of cortical neurons driven by the amblyopic eye were substantially and significantly lower than for neurons driven by the nonamblyopic eye. There were no reliable differences in neuronal contrast sensitivity between the eyes. A sample of neurons recorded from cortex representing the peripheral visual field showed no interocular differences, suggesting that the effects of amblyopia were more pronounced in portions of the cortex subserving foveal vision. Qualitatively, abnormalities in both the eye dominance and spatial properties of visual cortex neurons were related on a case-by-case basis to the depth of amblyopia. Quantitative analysis suggests, however, that these abnormalities alone do not explain the full range of visual deficits in amblyopia. Studies of extrastriate cortical areas may uncover further abnormalities that explain these deficits.

We analyzed the relationship between eye movements and neuronal responses recorded from area MT in alert monkeys trained to maintain visual fixation during the presentation of moving patterns. The monkeys made small saccades which moved the eyes with velocities that spanned the sensitivity range of MT neurons. The saccades evoked changes in the neuronal response that depended upon (1) the level of stimulus-evoked activity amidst which the saccade occurred and (2) the direction of the saccade relative to the preferred direction of the neuron. Most notably, saccades were able to suppress stimulus-evoked activity when they caused retinal image flow that opposed the neuron's preference and were able to elicit a response or enhance weak activity when they caused flow in the neuron's preferred direction. On average, the disturbance lasted 40 ms beginning about 40 ms following saccade onset. Using these parameters, we simulated synthetic spike trains from an imaginary pair of similarly tuned neurons and determined that the interneuronal correlation due to saccades should be negligible at all but the lowest ongoing firing rates. This conclusion was supported from our data by the observation that response variance for single MT spike trains was not measurably reduced during periods of stable gaze compared to periods when eye movement exceeded a stability criterion (0.1 deg during 0.5 s). While the intrusions caused by saccades are too short-lived and infrequent to account for the variability of MT neuronal response (counter to the finding in V1 of Gur et al., 1997), the clear directional signal that they carry in area MT suggests that motion perception is not blocked during saccades by suppression at early stages in the visual pathway.

In humans, esotropia of early onset is associated with a profound asymmetry in smooth pursuit eye movements. When viewing is monocular, targets are tracked well only when they are moving nasally with respect to the viewing eye. To determine whether this pursuit abnormality reflects an anomaly in cortical visual motion processing, we recorded eye movements and cortical neural responses in nonamblyopic monkeys made strabismic by surgery at the age of 10-60 d. Eye movement recordings revealed the same asymmetry in the monkeys' pursuit eye movements as in humans with early-onset esotropia. With monocular viewing, pursuit was much stronger for nasalward motion than for temporalward motion, especially for targets presented in the nasal visual field. However, for targets presented during ongoing pursuit, temporalward and nasalward image motion was equally effective in modulating eye movement. Single-unit recordings made from the same monkeys, under anesthesia, revealed that MT neurons were rarely driven binocularly, but otherwise had normal response properties. Most were directionally selective, and their direction preferences were uniformly distributed. Our neurophysiological and oculomotor measurements both suggest that the pursuit defect in these monkeys is not due to altered cortical visual motion processing. Rather, the asymmetry in pursuit may be a consequence of imbalances in the two eyes' inputs to the "downstream" areas responsible for the initiation of pursuit.