Modification of Peak Plasticity Induced by Brief Dark Exposure.

Kevin R Duffy,Nathan A Crowder,Donald E Mitchell,Alexander J Lingley

doi:10.1155/2019/3198285

Abstract

The capacity for neural plasticity in the mammalian central visual system adheres to a temporal profile in which plasticity peaks early in postnatal development and then declines to reach enduring negligible levels. Early studies to delineate the critical period in cats employed a fixed duration of monocular deprivation to measure the extent of ocular dominance changes induced at different ages. The largest deprivation effects were observed at about 4 weeks postnatal, with a steady decline in plasticity thereafter so that by about 16 weeks only small changes were measured. The capacity for plasticity is regulated by a changing landscape of molecules in the visual system across the lifespan. Studies in rodents and cats have demonstrated that the critical period can be altered by environmental or pharmacological manipulations that enhance plasticity at ages when it would normally be low. Immersion in complete darkness for long durations (dark rearing) has long been known to alter plasticity capacity by modifying plasticity-related molecules and slowing progress of the critical period. In this study, we investigated the possibility that brief darkness (dark exposure) imposed just prior to the critical period peak can enhance the level of plasticity beyond that observed naturally. We examined the level of plasticity by measuring two sensitive markers of monocular deprivation, namely, soma size of neurons and neurofilament labeling within the dorsal lateral geniculate nucleus. Significantly larger modification of soma size, but not neurofilament labeling, was observed at the critical period peak when dark exposure preceded monocular deprivation. This indicated that the natural plasticity ceiling is modifiable and also that brief darkness does not simply slow progress of the critical period. As an antecedent to traditional amblyopia treatment, darkness may increase treatment efficacy even at ages when plasticity is at its highest.

Highlights

Disruption of normal binocular vision during critical periods early in postnatal development can provoke anatomical and physiological alterations to neurons within the primary visual pathway
Monocular deprivation (MD) by eyelid closure can elicit a shift in cortical responsivity so that most neurons come to be excited only by stimulation of the nondeprived eye [1], leaving the deprived eye able to control few neurons and with a visual acuity deficit, called amblyopia [2], that is most severe in the central visual field [3]
This deprivation-induced shift in ocular dominance is consequent to a reduction in the number and strength of cortical neural connections serving the deprived eye [4,5,6], which is reflected by a reduction in the cross-sectional soma area of neurons within deprived-eye recipient layers of the dorsal lateral geniculate nucleus in the thalamus [7, 8]

Summary

Introduction

Disruption of normal binocular vision during critical periods early in postnatal development can provoke anatomical and physiological alterations to neurons within the primary visual pathway. The capacity of the visual system to be modified by imbalanced visual experience is regulated by age, reaching peak plasticity levels early in the postnatal life and thereafter declining through adolescence and into early adulthood [9,10,11,12]. The critical period for susceptibility to MD (Figure 1(a)) reaches its peak at about 4 weeks of age [9,10,11] and is followed by a decline to low levels by about 12-16 postnatal weeks [9, 10] followed again by an even slower decay to negligible levels at about 10 months [11, 12]. The capacity for recovery from the effects of MD likewise adheres to a critical period, but with a shorter timespan and with little recovery observed when MD is followed by reverse occlusion beyond about 12 weeks postnatal [13, 14]

Methods

Results

Conclusion