ObjectiveTo explore the dynamic changes of microvessels in the hippocampal CA3 area in mice model of temporal lobe epilepsy (TLE) induced by pilocarpine. MethodsEighteen health SPF male C57BL/6 mice were randomly divided into control group and status epilepticus (SE) group. The SE group was subdivided into three groups:SE-7 days, SE-28 days and SE-56 days. SE was induced by intraperitoneal injection of pilocarpine. And immunohistochemical staining was used to detected the localization of platelet endothelial cell adhesion molecule-1 (PECAM-1). ResultsIn the control group, PECAM-1 labeled microvessels arranged in a layered structure, and the microvessel of the orient layer was most prominent. After SE, the microvessels started to form an unorganized vascular plexus and appeared fibrous and fragmented, which was prominent at SE-28 days. Furthermore, the microvessels density increased the top at SE-28 days compared to the control (P < 0.001). ConclusionThe angiogenesis exists during the hippocampus formation in the mice model of TLE induced by pilocarpine, which could direct a new explanation for TLE formation and development.
ObjectiveTo explore the dynamic expression changes of neuronal growth and differentiation-associated miR-124a and miR-9 in the process of epileptogenesis. MethodsEstablish the lithium-pilocarpine induced status epilepticus (SE) rat model. Animal behavior change induced by SE as well as in the period of chronic epilepsy was observed by naked-eye or video-recording. Major time points for the study were chosen at 1d, 7d, 14d and 28d post-SE, on which the post-SE rats were decapitated and their hippocampal specimens were obtained. Total RNA from each specimen was extracted and qPCR was exploited to detect miR-124a and miR-9 expression in the specimens. Statistical analysis was used to show the dynamic expressional changes of miR-124a and miR-9 in rat hippocampus at 1d, 7d, 14d and 28d post-SE during the process of epileptogenesis. ResultsCompared with normal rats, the expression level of miR-124a in rat hippocampus did not show a significant difference at 1d post-SE, but it had shown markedly differences at 7d, 14d and 28d post-SE(P < 0.05), with a declining trend. Compared with normal rats, the expression level of miR-9 had demonstrated significant differences at 1d, 7d, 14d and 28d post-SE(P < 0.05)with a generally increasing trend, although there was slight fluctuation of expressional up-regulation at 7d post-SE. ConclusionNeuronal growth and differentiation-associated miR-124a and miR-9 had shown dynamic changes of down-regulation or up-regulation in the process of epileptogenesis. It can be suspected that miR-124a and miR-9 take part in hippocampal neurogenesis post-SE and be involved in epileptogenesis process.
ObjectiveImpaired breathing during and following seizures is an important cause of sudden unexpected death in epilepsy (SUDEP), but the network mechanisms by which seizures impair breathing have not been thoroughly investigated. Progress would be greatly facilitated by a model in which breathing could be investigated during seizures in a controlled setting. MethodRecent work with an acute Long-Evans rat model of limbic seizures has demonstrated that depression of brainstem arousal systems may be critical for impaired consciousness during and after seizures. We now utilize the same rat model to investigate breathing during partial seizures with secondary generalization. ResultBreathing is markedly impaired during seizures(P < 0.05;n=21), and that the severity of breathing impairment is strongly correlated with the extent of seizure propagation (Pearson R=-0.73;P < 0.001;n=30). ConclusionSeizure propagation could increase the severity of breathing impairment caused by seizures. Based on these results, we suggest that this animal model would help us to improve understanding of pathways involved in impairment of breathing caused by seizures and this is an important initial step in addressing this significant cause of SUDEP in people living with epilepsy.