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(Investigative Ophthalmology and Visual Science. 1999;40:2435-2439.)
© 1999 by The Association for Research in Vision and Ophthalmology, Inc.

Asymmetric Responses in Cortical Visually Evoked Potentials to Motion Are Not Derived from Eye Movements

James R. Wilson1, William W. Noyd1, Akhila D. Aiyer1, Anthony M. Norcia2, Michael J. Mustari3 and Ronald G. Boothe1

1 From the Yerkes Regional Primate Research Center, Departments of Cell Biology, Psychology, and Ophthalmology, Emory University, Atlanta, Georgia; 2 Smith-Kettlewell Eye Research Institute, San Francisco, California; and 3 Department of Anatomy and Neuroscience, University of Texas, Galveston.

Abstract

PURPOSE. Normal neonates and many adults after abnormal visual development have directional preferences for visual stimulus motions; i.e., they give better responses for optokinetic nystagmus (OKN) and visually evoked potentials (VEPs) in one direction than to those in the opposite direction. The authors tested whether the VEP responses were asymmetrical because of abnormal eye movements.

METHODS. VEPs were recorded from the visual cortices of five macaque monkeys: one normal, one neonate, and three reared with alternating monocular occlusion (AMO). They were lightly anesthetized, followed by paralysis to prevent eye movements. They then had "jittered" vertical grating patterns presented in their visual fields. The steady state VEPs were analyzed with discrete Fourier transforms to obtain the amplitudes and phases of the asymmetries.

RESULTS. The normal, control monkey had small, insignificant amplitudes of its asymmetrical Fourier component and random phases that were not 180o out of phase across the left and right eyes. The neonatal monkey and the AMO monkeys all had large, significant asymmetries that were approximately 180o out of phase between the left and right eyes.

CONCLUSIONS. The neonate and abnormally reared monkeys continued to have asymmetrical responses even after their eyes were paralyzed. Therefore, eye movements cannot be the source of the asymmetrical amplitudes of the VEPs, and the visual cortex is at least one source responsible for asymmetries observed in neonates and adults reared under abnormal visual inputs.




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