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Balsor, J.

Publications and source records attributed to Balsor, J..

2 recordsLinked to original sources

Constructing plasticity phenotypes to classify experience-dependent development of the visual cortex

Many neural mechanisms regulate experience-dependent plasticity in the visual cortex (V1) and new techniques for quantifying large numbers of proteins or genes are transforming how plasticity is studied into the era of big data. With those large data sets comes the challenge of extracting biologically meaningful results about visual plasticity from data-driven analytical methods designed for high-dimensional data. In other areas of neuroscience, high-information content methodologies are revealing more subtle aspects of neural development and individual variations that give rise to a richer picture of brain disorders. We have developed an approach for studying V1 plasticity that takes advantage of the known functions of many synaptic proteins for regulating visual plasticity and using that to rebrand the results of high-dimensional analyses into a plasticity phenotype. Here we provide a primer for analyzing experience-dependent plasticity in V1 using example R code to identify high-dimensional changes in a group of proteins. We describe using PCA to classify high-dimensional plasticity features and use them to construct a plasticity phenotype. In the examples, we show how the plasticity phenotype can be visualized and used to identify neurobiological features in V1 that change during development or after different visual rearing conditions. We include an R package "v1hdexplorer" that aggregates the various coding packages and custom visualization scripts written in R Studio.

neuroscience

Classification of visual cortex plasticity phenotypes following treatment for amblyopia

Monocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyopia. Less is known, however, about treatment-induced changes to those receptors and if those changes differentiate treatments that support the recovery of acuity versus persistent acuity deficits. Here we use an animal model to explore the effects of 3 visual treatments started during the CP (n=24, 10 male and 14 female); binocular vision (BV) that promotes good acuity versus reverse occlusion (RO) and binocular deprivation (BD) that causes persistent acuity deficits. We measured recovery of a collection of glutamatergic and GABAergic receptor subunits in V1 and modeled recovery of kinetics for NMDAR and GABAAR. There was a complex pattern of protein changes that prompted us to develop an unbiased data-driven approach for these high-dimensional data analyses to identify plasticity features and construct plasticity phenotypes. Cluster analysis of the plasticity phenotypes suggests that BV supports adaptive plasticity while RO and BD promote a maladaptive pattern. The RO plasticity phenotype appeared more similar to adults with high expression of GluA2 and the BD phenotypes were dominated by GABAA1, highlighting that multiple plasticity phenotypes can underlie persistent poor acuity. After 2-4 days of BV the plasticity phenotypes resembled normals, but only one feature, the GluN2A:GluA2 balance, returned to normal levels. Perhaps, balancing Hebbian (GluN2A) and homeostatic (GluA2) mechanisms is necessary for the recovery of vision.

neuroscience