当前位置: X-MOL 学术Neuroscience › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Aquaporin-4 Dysregulation in a Controlled Cortical Impact Injury Model of Posttraumatic Epilepsy.
Neuroscience ( IF 2.9 ) Pub Date : 2019-12-19 , DOI: 10.1016/j.neuroscience.2019.12.006
Jenny I Szu 1 , Som Chaturvedi 1 , Dillon D Patel 1 , Devin K Binder 1
Affiliation  

Posttraumatic epilepsy (PTE) is a long-term negative consequence of traumatic brain injury (TBI) in which recurrent spontaneous seizures occur after the initial head injury. PTE develops over an undefined period during which circuitry reorganization in the brain causes permanent hyperexcitability. The pathophysiology by which trauma leads to spontaneous seizures is unknown and clinically relevant models of PTE are key to understanding the molecular and cellular mechanisms underlying the development of PTE. In the present study, we used the controlled-cortical impact (CCI) injury model of TBI to induce PTE in mice and to characterize changes in aquaporin-4 (AQP4) expression. A moderate-severe TBI was induced in the right frontal cortex and video-electroencephalographic (vEEG) recordings were performed in the ipsilateral hippocampus to monitor for spontaneous seizures at 14, 30, 60, and 90 days post injury (dpi). The percentage of mice that developed PTE were 13%, 20%, 27%, and 14% at 14, 30, 60, and 90 dpi, respectively. We found a significant increase in AQP4 in the ipsilateral frontal cortex and hippocampus of mice that developed PTE compared to those that did not develop PTE. Interestingly, AQP4 was found to be mislocalized away from the perivascular endfeet and towards the neuropil in mice that developed PTE. Here, we report for the first time, AQP4 dysregulation in a model of PTE which may carry significant implications for epileptogenesis after TBI.

中文翻译:

创伤后癫痫的可控制的皮质撞击损伤模型中的水通道蛋白4失调。

创伤后癫痫病(PTE)是颅脑外伤(TBI)的长期负面结果,在颅脑外伤后会反复发作自发性癫痫发作。PTE在不确定的时期内发展,在此期间大脑中的电路重组会引起永久性的过度兴奋。创伤导致自发性癫痫发作的病理生理机制是未知的,PTE的临床相关模型是了解PTE发生基础的分子和细胞机制的关键。在本研究中,我们使用TBI的皮质控制冲击(CCI)损伤模型来诱导小鼠PTE并表征aquaporin-4(AQP4)表达的变化。在右额皮质诱导中度重度TBI,并在同侧海马中进行视频脑电图(vEEG)记录,以监测伤后(dpi)第14、30、60和90天的自发性癫痫发作。在14、30、60和90 dpi时,发生PTE的小鼠百分比分别为13%,20%,27%和14%。我们发现与不发育PTE的小鼠相比,在发育PTE的小鼠的同侧额叶皮层和海马中AQP4显着增加。有趣的是,在发育为PTE的小鼠中,发现AQP4的位置远离血管周围的末端,而朝向神经纤维。在这里,我们首次报道PTE模型中的AQP4失调,这可能对TBI后的癫痫发生产生重大影响。在14、30、60和90 dpi时,发生PTE的小鼠百分比分别为13%,20%,27%和14%。我们发现与不发育PTE的小鼠相比,在发育PTE的小鼠的同侧额叶皮层和海马中AQP4显着增加。有趣的是,在发育为PTE的小鼠中,发现AQP4的位置远离血管周围的末端,而朝向神经纤维。在这里,我们首次报道PTE模型中的AQP4失调,这可能对TBI后的癫痫发生产生重大影响。在14、30、60和90 dpi时,发生PTE的小鼠百分比分别为13%,20%,27%和14%。我们发现与不发育PTE的小鼠相比,在发育PTE的小鼠的同侧额叶皮层和海马中AQP4显着增加。有趣的是,在发育为PTE的小鼠中,发现AQP4的位置远离血管周围的末端,而朝向神经纤维。在这里,我们首次报道PTE模型中的AQP4失调,这可能对TBI后的癫痫发生产生重大影响。在发育为PTE的小鼠中,发现AQP4的位置远离血管周围的末端,而朝向神经纤维。在这里,我们首次报道PTE模型中的AQP4失调,这可能对TBI后的癫痫发生产生重大影响。在发育为PTE的小鼠中,发现AQP4的位置远离血管周围的末端,而朝向神经纤维。在这里,我们首次报道PTE模型中的AQP4失调,这可能对TBI后的癫痫发生产生重大影响。
更新日期:2019-12-20
down
wechat
bug