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G W Maguire, E L Smith, R S Harwerth, M L Crawford; Optically induced anisometropia in kittens.. Invest. Ophthalmol. Vis. Sci. 1982;23(2):253-264.
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Anisometropia was simulated in 11 kittens during the critical period of visual system development by securing a high-powered minus lens in front of one eye. Behavioral determinations of monocular grating acuity indicated that the induced refractive error resulted in severe amblyopia in the defocused eye. Microelectrode recordings in striate cortex revealed that the deficits in visual acuity were paralleled by a decrease in binocularly innervated neurons and a marked shift in ocular dominance toward the nondeprived eye. "Position of paralysis" estimates revealed that all the anisometropic kittens exhibited anomalous interocular alignments that were indicative of estropia. There was also a significant reduction in the cross-sectional areas of dorsal lateral geniculate nucleus (LGNd) neurons in laminae innervated by the deprived eye. A 6 week period of binocular recovery initiated when three of the anisometropic kittens were approximately 16 weeks of age resulted in a partial recovery of visual acuity; however, there was little or no evidence for recovery of cortical binocularity, cortical ocular dominance, LGNd neuron cell size, or interocular alignment. In general the visual system alterations produced by the induced anisometropia appear to be qualitatively similar to the anomalies associated with prolonged unilateral lid suture.
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