Spatio-temporal expression study of phosphorylated 70-kDa ribosomal S6 kinase (p70S6k) in mesial temporal lobe epilepsy / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To determine the spatio-temporal expression of p70S6k activation in hippocampus in mesial temporal lobe epilepsy.</p><p><b>METHODS</b>Temporal lobe epilepsy model was established by stereotaxically unilateral and intrahippocampal injection of kainite acid (KA) in adult male C57BL/6 mice. Latent and chronic epileptogenesis were represented by mice 5 days after KA injection (n = 5) and mice 5 weeks after KA injection (n = 8), respectively. Control mice (n = 5) were injected with saline. Immunohistochemical assays were performed on brain sections of the mice.</p><p><b>RESULTS</b>Hippocampus both ipsilateral and contralateral to the KA injection displayed significantly up-regulated pS6 immunoreactivity in dispersed granule cells in 5-day and 5-week model mice.</p><p><b>CONCLUSION</b>The activation of p70S6k is mainly located in the dentate gyrus in KA-induced mouse model of temporal lobe epilepsy, indicating that the activation may be related with the disperse degree and hypertrophy of granule cells.</p>

Role of beta-catenin in the pathogenesis of mesial temporal lobe epilepsy / 中国医学科学院学报

<p><b>OBJECTIVE</b>To explore the role of beta-catenin in the pathogenesis of mesial temporal lobe epilepsy.</p><p><b>METHODS</b>Kainic 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.</p><p><b>RESULTS</b>The 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.</p><p><b>CONCLUSION</b>Beta-catenin may not be involved in the development of hippocampal sclerosis of mesial temporal lobe epilepsy.</p>