Timing of the critical period for plasticity of ocular dominance columns in macaque striate cortex.
Visual deprivation induced by monocular eyelid suture, a laboratory model for congenital cataract, results in shrinkage of ocular dominance columns serving the closed eye. We performed monocular suture in macaques at ages 1, 3, 5, 7, and 12 weeks to define the critical period for plasticity of ocular dominance columns. After a minimum survival of 8 months, complete montages of [3H]proline-labeled columns were reconstructed from flat-mounts of striate cortex in both hemispheres. In any given monkey, visual deprivation induced the columns throughout striate cortex (V1) to retract the same distance from their original borders in layer IVcbeta. After deprivation, the widest columns remained in the foveal representation and along the V1/V2 border, where columns are widest in control animals. The narrowest deprived columns belonged to the ipsilateral eye, especially along the horizontal meridian and in the periphery, where columns are narrowest in control animals. At the earliest age that we tested (1 week), visual deprivation reduced the columns to fragments. These fragments always coincided with a cytochrome oxidase patch, or a short string of patches, in the upper layers. More severe column shrinkage occurred in layer IVcbeta (parvo) than layer IVcalpha (magno). The geniculate input to the patches in layer III (konio) appeared normal after deprivation, despite loss of CO activity. Surprisingly, the blind spot representation of the open eye was shrunken by monocular deprivation, although binocular competition is absent in this region. Our principal finding was that eyelid suture at age 1 week caused the most severe column shrinkage. With suture at later ages, the degree of column shrinkage showed a progressive decline. Deprivation commencing at age 12 weeks caused no column shrinkage. These results imply that primate visual cortex is most vulnerable to deprivation during the first weeks of life. Our experiments should provide further impetus for the treatment of children with congenital cataract at the earliest possible age.
Horton
J C
JC
Beckman Vision Center, University of California, San Francisco, San Francisco, California 94143-0730, USA.
Hocking
D R
DR
D000367:Age Factors; D000550:Amblyopia / Q000503:physiopathology; D000818:Animals; D001345:Autoradiography; D003423:Critical Period, Psychological; D003576:Electron Transport Complex IV / Q000032:analysis; D005260:Female; D005829:Geniculate Bodies / Q000166:cytology / Q000201:enzymology; D008252:Macaca fascicularis; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D012683:Sensory Deprivation / Q000502:physiology; D015349:Vision, Monocular / Q000502:physiology; D014793:Visual Cortex / Q000166:cytology* / Q000201:enzymology / Q000254:growth & development*; D014795:Visual Pathways / Q000502:physiology
D003576:Electron Transport Complex IV