Rapid plasticity of binocular connections in developing monkey visual cortex (V1)

Abstract

The basic sets of cortical connections are present at birth in the primate visual system. The maintenance and refinement of these innate connections are highly dependent on normal visual experience, and prolonged exposure to binocularly uncorrelated signals early in life severely disrupts the normal development of binocular functions. However, very little is known about how rapidly these changes in the functional organization of primate visual cortex emerge or what are the sequence and the nature of the abnormal neural events that occur immediately after experiencing binocular decorrelation. In this study, we investigated how brief periods of ocular misalignment (strabismus) at the height of the critical period alter the cortical circuits that support binocular vision. After only 3 days of optically imposed strabismus, there was a striking increase in the prevalence of V1 neurons that exhibited binocular suppression, i.e., binocular responses were weaker than monocular responses. However, the sensitivity of these neurons to interocular spatial phase disparity was not significantly altered. These contrasting results suggest that the first significant change in V1 caused by early binocular decorrelation is binocular suppression, and that this suppression originates at a site(s) beyond where binocular signals are initially combined. interocular suppression ͉ long-range interactions ͉ macaque monkeys ͉ strabismus

Long-Term Motor and Sensory Outcomes After Early Surgery for Infantile Esotropia

“…This hypothesis is supported by the recent report of Zhang et al showing that periods of abnormal experience as brief as 3 days at certain critical stages of binocular sensory maturation can cause permanent disruption of binocular sensory function in a primate model of strabismus. 26 Given the common developmental ratio of 4:1 for human:monkey, these data suggest that durations as brief as 2 weeks during a critical maturational phase could potentially cause permanent deficits in fusion and stereopsis.…”

Protection against deprivation amblyopia depends on relative not absolute daily binocular exposure

“…Interestingly, daily periods of BE imposed on kittens that were sufficient to prevent amblyopia in all animals so far tested did not always protect against the development of stereoblindness (Mitchell et al, 2009). Binocular cortical circuits of infant monkeys and particularly the long-range horizontal connections in the superficial layers of V1 are known to be very fragile and easily disrupted by abnormal early visual exposure (Zhang et al, 2005). A similar fragility of binocular connections in kitten V1 (Trachtenberg & Stryker, 2001) combined with the possibility that they may be also less susceptible to protection from daily binocular exposure in both species may lead to differences in the protective effects of BE on visual acuity and stereoscopic vision.…”

Strabismus and the Oculomotor System: Insights from Macaque Models

“…In strabismus, the principal observation is the large-scale reduction of binocular cells in V1 and V2 (Crawford & von Noorden 1979a, Crawford et al 1984). Further, there is an overall reduction in disparity processing and an increase in suppressive binocular interactions in V1 (Mori et al 2002, Smith et al 1997, Zhang et al 2005). It is likely that these observed disruptions to binocularity and increased suppression in the visual cortex result in cascading disruptions throughout the visual oculomotor system and, ultimately, lead to eye misalignment and eye movement abnormalities in addition to visual sensory deficits.…”