Abstract
During brain development, the neocortex shows periods of enhanced plasticity, which enables the acquisition of knowledge and skills that we use and build on in adult life. Key to persistent modifications of neuronal connectivity and plasticity of the neocortex are molecular changes occurring at the synapse. Here we used isobaric tag for relative and absolute quantification to measure levels of 467 synaptic proteins in a well-established model of plasticity in the mouse visual cortex and the regulation of its critical period. We found that inducing visual cortex plasticity by monocular deprivation during the critical period increased levels of kinases and proteins regulating the actin-cytoskeleton and endocytosis. Upon closure of the critical period with age, proteins associated with transmitter vesicle release and the tubulin- and septin-cytoskeletons increased, whereas actin-regulators decreased in line with augmented synapse stability and efficacy. Maintaining the visual cortex in a plastic state by dark rearing mice into adulthood only partially prevented these changes and increased levels of G-proteins and protein kinase A subunits. This suggests that in contrast to the general belief, dark rearing does not simply delay cortical development but may activate signaling pathways that specifically maintain or increase the plasticity potential of the visual cortex. Altogether, this study identified many novel candidate plasticity proteins and signaling pathways that mediate synaptic plasticity during critical developmental periods or restrict it in adulthood.
Highlights
Plasticity in the neocortex allows us to learn and adapt to our environment and occurs with active training and passive exposure
Identification of Proteins Affected by Monocular Deprivation, Age, or Dark Rearing Using isobaric tag for relative and absolute quantitation (iTRAQ)—In order to identify synaptic proteins involved in mediating ocular dominance (OD) plasticity in the visual cortex or regulating its critical period, we performed quantitative proteomics using iTRAQ on fractions containing synaptic membranes derived from the binocular visual cortex from groups of mice kept under four different experimental conditions (Fig. 1A)
This study provides a comprehensive insight into the changes in levels of synaptic membrane proteins that accompany OD plasticity in the visual cortex
Summary
V1, primary visual cortex; iTRAQ, isobaric tag for relative and absolute quantitation; MD, monocular deprivation; OD, ocular dominance; FDR, false discovery rate; ECM, extracellular matrix. The Synaptic Proteome during Visual Plasticity mass spectrometry We used this approach to identify proteins in the synaptic membrane fraction whose levels are altered by visual experience or age. We analyzed the synaptic membrane proteome of the binocular area of V1 from mice: (i) during the critical period, (ii) during the critical period while OD plasticity was being induced, (iii) in young adult mice after the critical period, and (iv) in young adult mice in which the critical period was delayed with dark rearing Direct comparison of these groups enabled us to study the effects of monocular deprivation and age on the synaptic membrane proteome fraction and analyze how dark rearing affected the age-induced changes
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