条件性敲除 TrkC 并不改变边缘性癫痫发生。
Conditional deletion of TrkC does not modify limbic epileptogenesis.
机构信息
Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
出版信息
Epilepsy Res. 2012 Nov;102(1-2):126-30. doi: 10.1016/j.eplepsyres.2012.07.019. Epub 2012 Sep 12.
Abstract
The neurotrophin receptor, tropomyosin-related kinase B (TrkB), is required for epileptogenesis in the kindling model. The role of a closely related neurotrophin receptor, TrkC, in limbic epileptogenesis is unknown. We examined limbic epileptogenesis in the kindling model in TrkC conditional null mice, using a strategy that previously established a critical role of TrkB. Despite elimination of TrkC mRNA, no differences in development of kindling were detected between TrkC conditional null and wild type control mice. These findings reinforce the central role of TrkB as the principal neurotrophin receptor involved in limbic epileptogenesis.
摘要
神经营养因子受体，原肌球蛋白相关激酶 B（TrkB），是点燃模型中癫痫发生所必需的。与之密切相关的神经营养因子受体 TrkC 在边缘性癫痫发生中的作用尚不清楚。我们使用先前确定 TrkB 关键作用的策略，在 TrkC 条件性缺失小鼠中检查了点燃模型中的边缘性癫痫发生。尽管消除了 TrkC mRNA，但在 TrkC 条件性缺失和野生型对照小鼠之间未检测到点燃发展的差异。这些发现加强了 TrkB 作为参与边缘性癫痫发生的主要神经营养因子受体的核心作用。
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