August 2014
Volume 14, Issue 10
Free
Vision Sciences Society Annual Meeting Abstract  |   August 2014
Abnormal surround suppression in amblyopic macaques
Author Affiliations
  • L.E. Hallum
    Center for Neural Science, New York University
  • N.J. Majaj
    Center for Neural Science, New York University
  • C. Shooner
    Center for Neural Science, New York University
  • R.D. Kumbhani
    Center for Neural Science, New York University
  • C.M. Ziemba
    Center for Neural Science, New York University
  • J.A. Movshon
    Center for Neural Science, New York University
  • L. Kiorpes
    Center for Neural Science, New York University
Journal of Vision August 2014, Vol.14, 688. doi:10.1167/14.10.688
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      L.E. Hallum, N.J. Majaj, C. Shooner, R.D. Kumbhani, C.M. Ziemba, J.A. Movshon, L. Kiorpes; Abnormal surround suppression in amblyopic macaques. Journal of Vision 2014;14(10):688. doi: 10.1167/14.10.688.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Amblyopia is a developmental disorder causing form vision deficits in the affected eye. Human psychophysics has shown that the representations of both luminance-defined and contrast-defined "2nd-order" forms are affected. Neurons in V1 and V2 of normal macaques typically show surround suppression (SS): the response to a grating is attenuated when the grating extends beyond the classical receptive field, stimulating the extraclassical surround. Since SS confers 2nd-order sensitivity to neurons, we wondered whether SS in amblyopic macaque V1/V2 would be abnormal. We analyzed data collected from 96-electrode "Utah" arrays implanted near the putative V1/V2 border at two eccentricities (0.5-3.0 deg) in each hemisphere of three anesthetized macaques (one control, two strabismic amblyopes). RFs were stimulated using (1) a grating presented through a circular aperture of varying diameter ("area summation"), and (2) large contrast-modulated (CM) gratings presented to both eyes simultaneously. Grating SF and orientation were selected based on preliminary measurements to vigorously drive overall responses. We quantified SS using an index: SSI = (Rp-Rf)/(Rp-Rb), where Rp, Rf and Rb are peak response, response to a full-diameter aperture, and response to a uniform, mean-luminance field, respectively. We used area summation responses to estimate the SSI in the eye ipsilateral (SSIi) and contralateral (SSIc) to array implantation. We ensured that the comparison between median SSIi and SSIc was not biased by the relative position of stimuli in each eye. In the control, SSIi was greater than SSIc: 0.54 versus 0.41 (p <0.05 Wilcoxon rank sum test). This difference was smaller in the mild strabismic: 0.57 versus 0.52, and reversed in the deep strabismic: 0.26 versus 0.64 (p <0.05). Our data suggest that SS is abnormal in amblyopic V1/V2, and this abnormality may underlie reported deficits in 2nd-order form perception.

Meeting abstract presented at VSS 2014

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