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A.M. Wong, A. Burkhalter, L. Tychsen; Neuroanatomic Mechanism for Suppression of the Non-Dominant Eye in Striate Cortex of Amblyopic/Strabismic Monkey: Role of Inhibitory Horizontal Connections . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4826.
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Purpose: Monocular deprivation and infantile strabismus can lead to the suppression of vision in the non-dominant eye. The purpose of this study was to test whether suppression induced by early monocular deprivation and strabismus affects the GABAergic innervation of horizontally projecting pyramidal cells in primary visual cortex (V1). Methods: A macaque monkey was monocularly deprived at age 3 weeks for 1 year causing monocular amblyopia and secondary infantile esotropia. At adult age, pyramidal cells that link ocular dominance columns (ODCs) were retrogradely labeled by injection of biotinylated dextran amine (BDA) in to single ODCs of V1 and visualized with a green fluorescent tag. ODCs that contained labeled cell bodies were identified 2 days after laser ablation of the left optic nerve head and visualization of cytochrome oxidase activity in V1. Inhibitory inputs to pyramidal cells were revealed by red immunofluorescent labeling of glutamic acid decarboxylase (GAD)–containing boutons apposed to BDA labeled somata. One normal adult animal served as control. The mean density of GAD-labeled boutons per pyramidal cell body circumference was calculated. Results: In ODCs connected to the deprived (amblyopic, nondominant) eye, the density of GAD-labeled boutons terminating on pyramidal neurons was substantially increased (p<.01). In ODCs connected to the normal, nondeprived dominant eye, the density of GAD-labeled boutons terminating on pyramidal neurons was equivalent to that in the ODCs of the control animal. Counts of the number of GAD boutons distributed throughout the ODCs, apposed to pyramidal or non-pyramidal neurons, revealed that the overall number of GAD boutons was similar in the amblyopic/strabismic and normal monkey ODCs. The increased density on pyramidal neurons observed in the deprived ODCs was due to a neuron-specific redistribution of GAD boutons and not an increase in absolute number. Conclusions: Intracortical suppression of the non-dominant eye in amblyopia/strabismus appears to be mediated by inhibitory, GABA-ergic neurons from the dominant eye which project (GAD boutons) onto excitatory, pyramidal neurons of the nondominant eye. These results elucidate further the role of horizontal connections (excitatory and inhibitory) within area V1. These horizontal connections allow binocular fusion when development is normal, and mediate interocular suppression when binocularity is maldeveloped.
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