Population representation of visual information in areas V1 and V2 of amblyopic macaques

被引:44
|
作者
Shooner, Christopher [1 ]
Hallum, Luke E. [1 ]
Kumbhani, Romesh D. [1 ]
Ziemba, Corey M. [1 ]
Garcia-Manin, Virginia [1 ]
Kelly, Jenna G. [1 ]
Majaj, Najib J. [1 ]
Movshon, J. Anthony [1 ]
Kiorpes, Lynne [1 ]
机构
[1] NYU, Ctr Neural Sci, New York, NY 10003 USA
关键词
Amblyopia; Ocular dominance; Visual cortex; Contrast sensitivity; OCULAR DOMINANCE COLUMNS; STRIATE CORTEX; CONTRAST SENSITIVITY; EXPERIMENTAL STRABISMUS; CORTICAL INHIBITION; CRITICAL-PERIOD; VERNIER ACUITY; MONKEYS; FIELD; PLASTICITY;
D O I
10.1016/j.visres.2015.01.012
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Amblyopia is a developmental disorder resulting in poor vision in one eye. The mechanism by which input to the affected eye is prevented from reaching the level of awareness remains poorly understood. We recorded simultaneously from large populations of neurons in the supragranular layers of areas V1 and V2 in 6 macaques that were made amblyopic by rearing with artificial strabismus or anisometropia, and 1 normally reared control. In agreement with previous reports, we found that cortical neuronal signals driven through the amblyopic eyes were reduced, and that cortical neurons were on average more strongly driven by the non-amblyopic than by the amblyopic eyes. We analyzed multiunit recordings using standard population decoding methods, and found that visual signals from the amblyopic eye, while weakened, were not degraded enough to explain the behavioral deficits. Thus additional losses must arise in downstream processing. We tested the idea that under monocular viewing conditions, only signals from neurons dominated by - rather than driven by - the open eye might be used. This reduces the proportion of neuronal signals available from the amblyopic eye, and amplifies the interocular difference observed at the level of single neurons. We conclude that amblyopia might arise in part from degradation in the neuronal signals from the amblyopic eye, and in part from a reduction in the number of signals processed by downstream areas. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:56 / 67
页数:12
相关论文
共 50 条
  • [1] Comparison of the angle representation in macaque visual areas V1 and V2
    Ito, Minami
    Komatsu, Hidehiko
    NEUROSCIENCE RESEARCH, 2006, 55 : S55 - S55
  • [2] VISUAL LATENCIES IN AREAS V1 AND V2 OF THE MACAQUE MONKEY
    NOWAK, LG
    MUNK, MHJ
    GIRARD, P
    BULLIER, J
    VISUAL NEUROSCIENCE, 1995, 12 (02) : 371 - 384
  • [3] COMPARISON OF STEREOSCOPIC MECHANISMS IN CORTICAL VISUAL AREAS V1 AND V2 OF CAT
    CLARKE, PGH
    WHITTERIDGE, D
    JOURNAL OF PHYSIOLOGY-LONDON, 1977, 272 (01): : P92 - P93
  • [4] ORGANIZATION OF THE CALLOSAL CONNECTIONS OF VISUAL AREAS V1 AND V2 IN THE MACAQUE MONKEY
    KENNEDY, H
    DEHAY, C
    BULLIER, J
    JOURNAL OF COMPARATIVE NEUROLOGY, 1986, 247 (03) : 398 - 415
  • [5] RESPONSE LATENCIES OF VISUAL CELLS IN MACAQUE AREAS V1, V2 AND V5
    RAIGUEL, SE
    LAGAE, L
    GULYAS, B
    ORBAN, GA
    BRAIN RESEARCH, 1989, 493 (01) : 155 - 159
  • [6] Neural mechanisms for cyclopean form perception in areas V1 and V2 of visual cortex
    Friedman, H
    Zhou, H
    Poggio, G
    vonderHeydt, R
    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 1996, 37 (03) : 1960 - 1960
  • [7] Less segregated processing of visual information in V2 than in V1 of the monkey visual cortex
    Tamura, H
    Sato, H
    Katsuyama, N
    Hata, Y
    Tsumoto, T
    EUROPEAN JOURNAL OF NEUROSCIENCE, 1996, 8 (02) : 300 - 309
  • [8] Functional interactions between areas V1 and V2 in the monkey
    Bullier, J
    Hupe, JM
    James, A
    Girard, P
    JOURNAL OF PHYSIOLOGY-PARIS, 1996, 90 (3-4) : 217 - 220
  • [9] Cortical dynamics of grouping and segregation in areas V1 and V2
    Ross, WD
    Grossberg, S
    Mingolla, E
    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 1996, 37 (03) : 1349 - 1349
  • [10] CALLOSAL CONNECTIVITY OF AREAS V1 AND V2 IN THE NEWBORN MONKEY
    DEHAY, C
    KENNEDY, H
    BULLIER, J
    JOURNAL OF COMPARATIVE NEUROLOGY, 1986, 254 (01) : 20 - 33