OBJECTIVETo explore the role of beta-catenin in the pathogenesis of mesial temporal lobe epilepsy.

METHODSKainic acid-induced rat models of medial temporal lobe epilepsy was established. The expression of beta-catenin in the normal mice and the model mice were detected using Western blot analysis. The expression of beta-catenin at human hippocampus was detected using immunohistochemical analysis and immunofluorescence and compared between patients with non-hippocampal sclerosis temporal lobe epilepsy and those with hippocampal sclerosis epilepsy.

RESULTSThe pathologies of model mice were similar with those in mice with hippocampal sclerosis temporal lobe epilepsy, demonstrating that the mice model was successfully established. Western blot analysis showed no significant difference of beta-catenin expression between normal mice and model mice. As shown by immunohistochemical analysis and immunofluorescence, beta-catenin expression in human hippocampus was also not significantly different between patients with temporal lobe epilepsy without hippocampal sclerosis and those with hippocampal sclerosis.

CONCLUSIONBeta-catenin may not be involved in the development of hippocampal sclerosis of mesial temporal lobe epilepsy.