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Abnormal response dynamics of V2 neurons in amblyopic monkeys



Conference Title

Society of Neuroscience Annual Meeting


Society of Neuroscience


Washington, D.C. / November 15-19, 2014

Publication Date / Copyright Date



The maturation of the primate visual brain depends on normal visual experience and requires precise matching of images in the two eyes. Experiencing interocular decorrelation of cortical input signals early in life, because of early ocular misalignment (strabismus) or monocular defocus (anisometropia), is known to often cause amblyopia. Amblyopic subjects typically show reductions in contrast sensitivity and visual acuity in their affected eye but also exhibit a broad range of far more complex spatial vision deficits. Thus amblyopia is often described as a developmental vision disorder of spatial vision. However, an increasing number of perceptual studies on amblyopia indicate that temporal signal processing in the amblyopic visual brain may be also abnormal. Therefore we created several primate models of anisometropic amblyopia by rearing infant monkeys with defocusing lens between 3 weeks and 3 months of age. Following the behavioral assessment of their visual capacities, we studied the temporal patten (dynamics) of V2 neurons’s responses to brief (640 msec) high-contrast (80%) stationary gratings that were optimized in each unit for spatial frequency, orientation, and spatial phase (for simple cells). We measured the onset latency, the onset-to-peak latency, and the response decay. We found that 1) the onset latency of V2 neurons driven by the amblyopic eye was significantly shorter than that for neurons driven by the fellow eye or that for neurons from normal monkeys, 2) there was no significant difference in the onset-to-peak latency between normal and amblyopic monkeys, and 3) the response decay time (time constant) was much longer in amblyopic neurons comapred to that in normal units. Taken together, the temporal patterns of firing in V2 neurons of amblyopic monkeys are substantially different from that in normal monkeys. The observed abnormal dynamics of spiking in amblyopic neurons may be related to some of the temporal vision deficits reported in human amblyopes.



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