The ELT is characterized by selective loss of neurons in the CA1 and CA3 subfields of the hippocampus, glial scar, dispersion in the dentate gyrus granule cells and mossy fiber sprouting. Studies to identify signaling pathways during epileptogenesis has shown that some routes involving both processes of neuronal death as neuroprotective agents, such as caspases. Caspases, Bim and Bax overexpression are considered pro-apoptotic, whereas Akt / PKB, Bcl-XL, calbindin and HSP 70 are anti-apoptotic molecules. Adenosine is a nucleoside that exerts anticonvulsant and neuroprotective, primarily through activation of A1 receptors. Its analogues may cause apoptosis or protect from cell death, by mechanisms still poorly understood. Previous studies in the pilocarpine model show that pretreatment with R-PIA reduces hippocampal neuronal death. Current studies have sought to identify molecules involved in the process of lesions present in the epileptic human tissue, and its expression in ELT model induced by pilocarpine with and without pretreatment with R-PIA. The objectives of this study are: 1) by proteomic analysis to investigate the proteins expressed in the hippocampus of TLE patients as well as in the hippocampus of rats submitted to pilocarpine model studied in the acute phase, latent and chronic; 2) determine the expression profile of these proteins by pre-treatment with R-PIA, 3) measure by Western blotting, and Bim Akt/Bcl-XL/HSP-70 / Bax / caspases in the hippocampus of rats treated with pilocarpine with or without R-PIA. Our interest is to understand the balance between pro and anti-apoptotic in ELT, and verify that the neuroprotective agent R-PIA is able to modulate some of these mechanisms.
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