Traumatic brain injury in mice lacking the K channel, TREK-1
Traumatic brain injury in mice lacking the K channel, TREK-1
复制标题
DOI：
10.1038/jcbfm.2010.223
复制
发表时间：
2011-03-01
影响因子：
6.3
通讯作者：
Bryan, Robert M., Jr.
中科院分区：
文献类型：
--
作者：
Namiranian, Khodadad;Brink, Christa D.;Bryan, Robert M., Jr.
本研究的目的是确定钾通道TREK-1是否在创伤性脑损伤（TBI）后具有神经保护作用。由于没有选择性阻断剂，我们使用TREK-1敲除（KO）小鼠进行研究。将野生型（WT）和TREK-1 KO小鼠麻醉并进行受控皮质撞击损伤（通过以3 m/s行进的3 mm直径杆使脑变形1.5mm）。在WT和TREK-1 KO小鼠中，损伤皮质中的激光多普勒灌注（LDP）降低了约80%，并保持在该水平（分别为n = 10和11）。激光多普勒血流灌注减少50%至60%，直接邻近损伤部位的皮质区。不同基因型间的LDP差异无统计学意义。在TBI后15天，使用苏木精和伊红染色的冠状脑切片确定的挫伤体积，WT和TREK-1 KO分别为4.1 ± 0.8（n = 10）和5.1 ± 0.5（n = 11）mm（3）（不显著，P = 0.34）。WT和TREK-1 KO小鼠之间海马CA 1和CA 3区域中存活神经元的细胞计数相似（对于CA 1和CA 3，分别为P = 0.51和0.84）。我们得出结论，TREK-1表达不提供脑保护后TBI。脑血流与代谢杂志（2011）31; doi：10.1038/jcbfm.2010.223; 2010年12月15日在线发表
The purpose of this study was to determine whether the potassium channel, TREK-1, was neuroprotective after traumatic brain injury (TBI). Since there are no selective blockers, we used TREK-1 knockout (KO) mice for our study. Wild-type (WT) and TREK-1 KO mice were anesthetized and subjected to controlled-cortical impact injury (deformation of the brain by 1.5mm by a 3-mm diameter rod traveling at a 3 m/s). Laser Doppler perfusion (LDP) decreased by similar to 80% in the injured cortex and remained at that level in both WT and TREK-1 KO mice (n = 10 and 11, respectively). Laser Doppler perfusion decreased by 50% to 60% in cortical areas directly adjacent to the site of injury. There were no statistical differences in LDP between genotype. The contusion volume, determined 15 days after the TBI using hematoxylin and eosin-stained coronal brain sections, was 4.1 +/- 0.8 (n = 10) and 5.1 +/- 0.5 (n = 11) mm(3) for WT and TREK-1 KO, respectively (not significant, P = 0.34). Cell counts of viable neurons in the CA1 and CA3 regions of the hippocampus were similar between WT and TREK-1 KO mice (P = 0.51 and 0.84 for CA1 and CA3, respectively). We conclude that TREK-1 expression does not provide brain protection after TBI. Journal of Cerebral Blood Flow & Metabolism (2011) 31; doi:10.1038/jcbfm.2010.223; published online 15 December 2010