Changes in KCNQ2 immunoreactivity in the amygdala in two rat models of temporal lobe epilepsy

Molecular Brain Research Pub Date : 2005-11-18 Epub Date: 2005-09-09 DOI:10.1016/j.molbrainres.2005.08.004

Silke Penschuck , Jesper F. Bastlund , Henrik Sindal Jensen , Tine Bryan Stensbol , Jan Egebjerg , William P. Watson

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引用次数: 14

Abstract

Potassium channels containing the KCNQ2 subunit play an important role in the regulation of neuronal excitability and therefore have been implicated in epilepsy. This study describes the expression of KCNQ2 subunit immunoreactivity in the basolateral amygdala in two rat models of temporal lobe epilepsy, (1) amygdala kindling and (2) spontaneously epileptic rats after status epilepticus induced by hippocampal electrical stimulation. KCNQ2 subunit immunoreactivity was assessed with a commercial antibody raised against a C-terminal part of the KCNQ2 protein. We show that KCNQ2 subunit immunoreactivity is upregulated in the basolateral amygdala in both models and that generalized seizures are required to induce this upregulation. We hypothesize that the upregulation of potassium channels containing the KCNQ2 subunit might represent a mechanism to counteract seizures in experimental temporal lobe epilepsy.

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两种颞叶癫痫大鼠杏仁核中KCNQ2免疫反应性的变化

含有KCNQ2亚基的钾通道在神经元兴奋性的调节中起重要作用，因此与癫痫有关。本研究描述了两种颞叶癫痫大鼠(1)杏仁核点燃模型和(2)海马电刺激诱导癫痫持续状态后自发性癫痫大鼠基底外侧杏仁核中KCNQ2亚基免疫反应性的表达。KCNQ2亚基免疫反应性通过针对KCNQ2蛋白c端部分的商业抗体进行评估。我们发现，在两种模型中，KCNQ2亚基免疫反应性在基底外侧杏仁核中上调，并且需要全身性癫痫发作来诱导这种上调。我们假设含有KCNQ2亚基的钾通道的上调可能代表了一种对抗实验性颞叶癫痫发作的机制。

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Molecular Brain Research

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