HMGB1, neuronal excitability and epilepsy

Abstract Epilepsy is a common neurological disease caused by synchronous firing of hyperexcitable neurons. Currently, anti-epileptic drugs remain the main choice to control seizure, but 30% patients are resistant drugs, which calls for more research on new promising targets. Neuroinflammation closely associated with development epilepsy. As an important inflammatory factor, high mobility group protein B1 (HMGB1) has shown elevated expression and increased proportion translocation from nucleus cytoplasm in epilepsy multiple animal models HMGB1 can act downstream receptors such as Toll-like receptor 4 advanced glycation end products, thereby activating interleukin (IL)-1β nuclear factor kappa-B (NF-κB), turn glutamate N-methyl-D-aspartate (NMDA) aggravate hyperexcitability The stimulate HMGB1. Blocking its signaling pathways may be direction antiepileptic drug therapy. Here, we review changes HMGB1-related pathway epileptic brains role modulation neuronal excitability seizure. Furthermore, discuss potentials therapeutic target provide perspective future