癫痫发作可诱导海马内脑源性神经营养因子 (BDNF)水平上调 ,进而激活海马门区及CA3区腔隙层的TrkB受体 ,通过促进兴奋性神经递质释放等效应加强海马通路尤其是苔状纤维的兴奋性突触传递 ,从而导致持续的高度兴奋状态 ;而阻断BDNF信号转导通路则可抑制癫痫发生。提示BDNF在癫痫发作过程中具有重要作用 ,进一步阐明其细胞分子机制将为探索癫痫治疗手段提供新途径 Epileptic seizures induce upregulation of brain-derived neurotrophic factor (BDNF) in the hippocampus, which in turn activates TrkB receptors in the lacunar and cavernous lacunae of the CA3 region and enhances the hippocampal pathway especially by increasing excitatory neurotransmitter release Excitatory synaptic transmission of fibrous fibers, resulting in a sustained high state of excitement; while blocking the BDNF signal transduction pathway can inhibit the occurrence of epilepsy. It is suggested that BDNF plays an important role in the process of epilepsy and further elucidates its molecular mechanism will provide a new way to explore the treatment of epilepsy