Modification of Peak Plasticity Induced by Brief Dark Exposure

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.

Aging increases lateral but not local inhibition of orientation processing in primary visual cortex

Aging-related declines in vision can decrease well-being of the elder. Concerning early sensory changes as in the primary visual cortex, physiological and behavioral reports seem contradictory. Neurophysiological studies on orientation tuning properties suggested that neuronal changes might come from decreased cortical local inhibition. However, behavioral results either showed no clear deficits in orientation processing in the elder, or proposed stronger surround suppression. Through psychophysical experiments conducted on old and young human subjects combined with computational modeling, we resolved these discrepancies by demonstrating stronger lateral inhibition in the elder while neuronal orientation tuning widths, related to local inhibition, stayed globally intact across age. We confirmed this later finding by re-analyzing published neurophysiological data from rhesus monkeys, which showed no systematic tuning width changes, but instead a higher neuronal noise with aging. These results suggest a stronger lateral inhibition and mixed effects on local inhibition during aging, revealing a more complex picture of age-related effects in the central visual system than previously thought.Significance StatementVisual functions decline during aging, adversely affecting quality of life. Much of this dysfunction is probably mediated by disturbances in the balance between inhibition and excitation in the central visual system. It was proposed that the inhibitory function within the aging visual cortex might be modified, but huge discrepancies exist among different reports. Here we identify the specific inhibitory circuit change, which has not been clearly evaluated, by using behavioral measures, neural modeling and re-analysis of non-human primate electrophysiological data. We provide evidence that a stronger lateral inhibition and mixed effects on local inhibition during aging, revealing a more complex picture of age-related effects in the central visual system than previously thought.Author contributionsZCW and TT designed and analyzed behavioral experiments; ZCW performed experiments; ZCW and TT performed data analysis and neurophysiological re-analysis; YS and FY provided physiological data and discussed its re-analysis; TT performed modeling; ZCW, YFZ and TT provided project supervision and funds; ZCW and TT wrote the paper; all authors discussed and commented on the manuscript.

Somatostatin-like immunoreactivity in the pigeon visual system: Developmental expression and effects of retina removal

The distribution of somatostatin (SS)-containing neurons was investigated by immunocytochemical methods in the central visual system of adult, developing, and retina-ablated pigeons. In normal adult brains, SS-positive cells and processes were present in the optic tectum, the nucleus of the basal optic root, the visual Wulst, and the ectostriatum. During development, progressive increase or decrease in the numerical density and the total number of SS-containing neurons occurred as determined by quantitative analysis. Changes in SS immunoreactivity also occurred as a consequence of unilateral and bilateral retina removal immediately after hatching, i.e. before retinofugal connections have been established. In spite of the segregation of visual inputs due to the almost completely crossed retinal projections, unilateral and bilateral deafferentation differentially affected SS-containing visual regions. In addition, different effects were observed on the relative packing density of labeled cells as compared to their total number. A possible role of retinal axons in regulating the distribution of SS immunoreactivity was suggested by its altered expression induced by retinal deafferentation. In addition, parallels with the distribution of SS immunoreactivity in the pigeon’s visual system were used to suggest possible equivalence between cell populations in the avian and the mammalian brains.