Ação da metilprednisolona no sistema nervoso central de roedores: viabilidade celular e envolvimento com memória

Abstract

Methylprednisolone (METP) is a synthetic glucocorticoid that has widespread and worldwide use in the clinical area. In addition to anti-inflammatory and immunological activity, glucocorticoids are also known to interfere in memory consolidation processes, but little is known about its mechanisms. Recently, glucocorticoid METP has been shown to induce a positive modulation of rodents neuromuscular transmission, which results in increased calcium influx at end plates. Knowing this, we propose that some mechanisms related to calcium-dependent signaling pathways may be involved also in the mnemonic response of glucocorticoids. The aim of this work was to investigate the effects of METP on cell viability and on cellular signaling element involved in memory, the calcium and calmodulin dependent protein kinase type II - CaMKII, in the central nervous system of rodents. The cell viability of cerebral slices treated with doses of 3, 30 and 300 μM METP was assayed using the MTT colorimetric test and the glucose and oxygen deprivation model (PGO). As for in vivo assays, hippocampal and cortex structures from rats treated with 5 mg/kg and 30 mg/kg of METP were subjected to 10% SDS-PAGE and Western blot technique. Results were analyzed by the ImageJ software (NIH). The use of animals was previously approved by the Committee on Ethics in Animal Use (CEUA / UNIPAMPA 037/2012). The results demonstrated an increase in the electrophoretic density and immunocontent of CaMKII in cortex in vivo METP treatment. In cortex and hippocampal slices, in vitro METP treatment, provided an increase in cell viability, but not related to neuroprotection, at least to ischemic events provided by glucose and oxygen deprivation. The data presented in this work suggest that memory enhancement induced by low dose METP treatment involves the calcium dependent signaling pathway of CaMKII.