Funny team member makes key plays, but leaves the dendritic field when hit hard.
Funny team member makes key plays, but leaves the dendritic field when hit hard.
复制标题
有趣的团队成员发挥了关键作用，但在遭受重创时离开了树突场。
DOI：
10.1111/j.1535-7511.2008.00257.x
复制
发表时间：
2008
影响因子：
3.6
通讯作者：
Cooper,EdwardC
中科院分区：
文献类型：
--
作者：
Cooper,EdwardC
大鼠匹罗卡品癫痫模型中癫痫发生过程中的进行性树突状HCN代谢病。Jung S，Jones TD，卢戈JN Jr，Sheerin AH，米勒JW，D 'Ambrosio R，安德森AE，Poolos NP。神经科学杂志2007;27（47）：13012-13021。离子通道病在具有遗传原因的人类癫痫中起重要作用，并且已经假设在获得性CNS损伤后的癫痫中也发生。在癫痫动物模型中，诱导癫痫持续状态（SE）后，离子通道功能发生获得性改变，但尚不清楚它们与自发性癫痫发作的关系。我们研究了超极化激活的阳离子（HCN）通道的性质，在CA 1海马锥体神经元结合视频脑电图（VEEG）记录监测自发性癫痫发作的发展，在大鼠匹罗卡品癫痫模型。我们的研究结果表明，树突状HCN通道显着下调，在急性时间点1周后毛果芸香碱，通道表达和电压依赖性激活的超极化的损失。当癫痫在慢性期建立时，这种下调逐渐增加。令人惊讶的是，在急性期的VEEG记录显示，相当一部分动物已经经历了反复发作。抑制这些癫痫发作与苯巴比妥逆转的变化，电压依赖性的Ih，电流产生的HCN通道，但不影响HCN通道表达的损失。这些结果表明两种机制的HCN通道下调后SE，一个依赖于和一个独立的反复发作。这种树突状HCN通道功能的早期和进行性下调增加了神经元的兴奋性，并可能与癫痫发生和维持癫痫状态的过程有关。
Progressive Dendritic HCN Channelopathy during Epileptogenesis in the Rat Pilocarpine Model of Epilepsy.Jung S, Jones TD, Lugo JN Jr, Sheerin AH, Miller JW, D'Ambrosio R, Anderson AE, Poolos NP.J Neurosci2007;27(47):13012–13021. Ion channelopathy plays an important role in human epilepsy with a genetic cause and has been hypothesized to occur in epilepsy after acquired insults to the CNS as well. Acquired alterations of ion channel function occur after induction of status epilepticus (SE) in animal models of epilepsy, but it is unclear how they correlate with the onset of spontaneous seizures. We examined the properties of hyperpolarization-activated cation (HCN) channels in CA1 hippocampal pyramidal neurons in conjunction with video-EEG (VEEG) recordings to monitor the development of spontaneous seizures in the rat pilocarpine model of epilepsy. Our results showed that dendritic HCN channels were significantly downregulated at an acute time point 1 week postpilocarpine, with loss of channel expression and hyperpolarization of voltage-dependent activation. This downregulation progressively increased when epilepsy was established in the chronic period. Surprisingly, VEEG recordings during the acute period showed that a substantial fraction of animals were already experiencing recurrent seizures. Suppression of these seizures with phenobarbital reversed the change in the voltage dependence ofIh, the current produced by HCN channels, but did not affect the loss of HCN channel expression. These results suggest two mechanisms of HCN channel downregulation after SE, one dependent on and one independent of recurrent seizures. This early and progressive downregulation of dendritic HCN channel function increases neuronal excitability and may be associated with both the process of epileptogenesis and maintenance of the epileptic state.