Department of Neurosurgery, Duke University Medical Center, Durham, NC, USA.
Department of Neurosurgery, Duke University Medical Center, Durham, NC, USA; Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
Neuropharmacology. 2020 May 1;167:107734. doi: 10.1016/j.neuropharm.2019.107734. Epub 2019 Aug 1.
Traumatic brain injury (TBI) and status epilepticus (SE) have both been linked to development of human epilepsy. Although distinct etiologies, current research has suggested the convergence of molecular mechanisms underlying epileptogenesis following these insults. One such mechanism involves the neurotrophin brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin related kinase B (TrkB). In this review, we focus on currently available data regarding the pathophysiologic role of BDNF/TrkB signaling in epilepsy development. We specifically examine the axonal injury and SE epilepsy models, two animal models that recapitulate many aspects of TBI- and SE-induced epilepsy in humans respectively. Thereafter, we discuss aspiring strategies for targeting BDNF/TrkB signaling so as to prevent epilepsy following an insult or suppress its expression once developed. This article is part of the special issue entitled 'New Epilepsy Therapies for the 21st Century - From Antiseizure Drugs to Prevention, Modification and Cure of Epilepsy'.
创伤性脑损伤 (TBI) 和癫痫持续状态 (SE) 都与人类癫痫的发生有关。尽管病因不同，但目前的研究表明，这两种损伤后致痫机制存在分子机制的趋同。其中一种机制涉及神经营养因子脑源性神经营养因子 (BDNF) 及其高亲和力受体原肌球蛋白相关激酶 B (TrkB)。在这篇综述中，我们重点关注目前关于 BDNF/TrkB 信号在癫痫发生中的病理生理作用的可用数据。我们特别研究了轴突损伤和 SE 癫痫模型，这两种动物模型分别模拟了 TBI 和 SE 诱导的人类癫痫的许多方面。之后，我们讨论了靶向 BDNF/TrkB 信号的有前途的策略，以便在损伤后预防癫痫或在其发生后抑制其表达。本文是题为“21 世纪的新癫痫治疗方法 - 从抗癫痫药物到癫痫的预防、修饰和治疗”的特刊的一部分。
