Aumento da ativação neuronal e de marcação de BDNF após degradação das redes perineuronais em modelo experimental de privação sensorial

Abstract

The central nervous system (CNS) has the ability to processing and store information collected from the environment, and modifies and adapt under environmental stimuli diversity. However, It has low regeneration capacity after injury or neurodegenerative disease. Several works are demonstrating cellular and molecular mechanisms implicated in CNS plasticity, such as chondroitin sulfate glycosaminoglycans (GAGs-SC) important components of the extracellular matrix from nervous tissue, responsible for synaptic stabilization, toconcentrateof growth factors and ions around neurons. Removing CSPG of the nervous tissue, we can (re)opens a potential plasticity window in the CNS. The goal of our work is to evaluate the influence of removal of GAGs-SC on neuronal activity, via cFos immunolabeling, and BDNF proteins levels at the barrel cortex, under an experimental model of sensory deprivation (vibrissectomy) during critical period of plasticity. To do that, we used 18 rats (Rattus novergicus), Wistar lineage, submitted to the removal of all whiskers from their right snout (vibrissectomy) since first day of life (P0) until the end of critical period of plasticity (P30). The 40 days deprived animals received epidural polimer implant of Elvax, previously saturated with chondroitinase ABC (ChABC, to degraded the extracellular matrix) or with bovine albumin serum(BSA, control), on the barrel cortex of contralateral cerebral hemisphere to the sensory deprivation (left). The animals were perfused 10 (P50) or 20 days (P60) after Elvax implant. Our results shown that the animals submitted to the sensory deprivation, during critical period of plasticity of S1, and to GAGsSC degradation presents modification in perineuronal net (PNNs) characteristics when compared to control animals, at P50. Those animals also presents increase in cFos labeled cells (mainly at the granular layer of S1) and in BDNF labeled cells at the deprived PMBSF, both seen in 10 (P50) as 20 days (P60) after Elvax implant saturated with ChABC. In this way, we concluded that GAGs-SC removal induced local plasticity, evoking changes in cortical activity and BDNF expression at the deprived PMBSF, even 30 days after critical period of plasticity ended at S1.