Abstract

In recent years, evidence has accumulated indicating that long-ranging neuronal connections within the primary visual cortex (area 17) mediate the influences of context and experience, possibly also those of expectation. After early onset strabismus, the layout of these connections is massively modified: in strabismic but not in normally raised cats, horizontal connections extend primarily between neurons activated by the same eye. As a possible consequence of the modified circuitry, neuronal synchronization between different ocular dominance domains is also massively reduced. Thus, the inability of strabismics to combine the signals arriving from the two eyes into a single percept may be caused by these structural and functional changes. Strabismic amblyopia is also accompanied by significant modifications of intracortical associational interactions: corresponding to the psychophysical deficits, neurons driven by the normal eye displayed stronger synchronization of their responses than neurons dominated by the amblyopic eye.¹ These data demonstrated for the first time a clear neurophysiological correlate of strabismic amblyopia in area 17. They suggest that – similar to our observations in divergent squinters – at least some of the perceptual deficits of amblyopic patients are due to experience-dependent changes in intracortical circuitry. We analyze this question by combining optical imaging of intrinsic signals with 3-D reconstructions of neuronal circuitry.

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