Haphazard neural connections underlie the visual deficits of cats with strabismic or deprivation amblyopia

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Abstract
Identification of the neural basis of the visual deficits experienced by humans with amblyopia, particularly when associated with strabismus (strabismic amblyopia), has proved to be difficult in part because of the inability to observe directly the neural changes at various levels of the human visual pathway. Much of our knowledge has necessarily been obtained on the basis of sophisticated psychophysical studies as well as from electrophysiological explorations on the visual pathways in animal models of amblyopia. This study combines these two approaches to the problem by employing similar psychophysical probes of performance on animal models of two forms of amblyopia (deprivation and strabismic) to those employed earlier on human amblyopes (Hess & Field, 1994, Vis. Res., 34, 13397–13406). The tests explore two competing explanations for the visual deficits, namely an evenly distributed loss of neural connections (undersampling) with the amblyopic eye as opposed to disordered connections with this eye (neural disarray). Unexpectedly, the results in animal models of deprivation amblyopia were not in accord with expectations based upon an even distribution of lost connections with the amblyopic eye. However, the results were similar to those observed in a strabismic amblyopic animal and to strabismic amblyopic humans. We suggest that deprivation amblyopia may be accompanied by an uneven loss of connections that results in effective neural disarray. By contrast, amblyopia associated with strabismus might arise from neural disarray of a different origin such as an alteration of intrinsic cortical connections.