Curso temporal da degradação e restauração de redes perineuronais após a ação da enzima chabc entregue via implante de biomembrana no córtex cerebral de ratos

Abstract

The chondroitin sulfate proteoglycans (CSPGs) founded on the extracellular matrix (ECM) of nervous tissue are the main components related to the restriction of neuroplasticity. When condenserd, they form the perineuronal nets (PNNs) and their appearance coincides with the end of the critical period of plasticity and reduction of the reorganization potencial of the central nervous system (CNS). The degradation of PNNs by the enzyme chondroitinase ABC has been used as a tool for reopening periods of neuroplasticity in adult nervous system.. In this work, we analyzed the temporal dynamics of PNNs degradation and restoration in the primary somesthetic cortex (S1) after degradation by the enzyme ChABC in an in vivo experimental model using a biomembrane vehicle for focal delivery and without damaging nervous tissue. In this way, we used adult Wistar rats that were submitted to the implantation of the biomembrane made with ethylene-vinyl-acetate saturated with the enzyme ChABC, with 1, 3 and 7 days of survival time after implantation, using the non implanted side cerebral hemisphere as a control. Our results demonstrated that degradation via implantation of the biomembrane saturated with ChABC was efficient from day 1, with a drastic reduction in the implanted hemisphere (LH) of mature PNNs. There was also a significant increase in the number of immature PNNs in the HD even 7 days after implantation. Neither the biomembrane or the enzyme triggered signs of a neuroinflammatory process or glial activation, but the removal of ECM components interfered with the immunostaining of nerve cells 7 days after the implantation of the biomembrane with ChABC. Therefore, we concluded that the ethylene-vinyl-acetate polymer biomembrane was efficient for focal delivery of the ChABC enzyme and promoted degradation of PNNs in the S1 area of adult rats, did not cause mechanical damage to the nervous tissue, nor activated glial reactivity and the area of enzymatic degradation decreases over time (from 1 to 7 days).