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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Protective role of K(v)7 channels in oxygen and glucose deprivation-induced damage in rat caudate brain slices
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Protective role of K(v)7 channels in oxygen and glucose deprivation-induced damage in rat caudate brain slices

机译：K（v）7通道在缺氧和葡萄糖剥夺诱导的大鼠尾脑切片中的保护作用

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摘要

Ischemic stroke can cause striatal dopamine efflux that contributes to cell death. Since K(v)7 potassium channels regulate dopamine release, we investigated the effects of their pharmacological modulation on dopamine efflux, measured by fast cyclic voltammetry (FCV), and neurotoxicity, in Wistar rat caudate brain slices undergoing oxygen and glucose deprivation (OGD). The K(v)7 activators retigabine and ICA27243 delayed the onset, and decreased the peak level of dopamine efflux induced by OGD; and also decreased OGD-induced damage measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Retigabine also reduced OGD-induced necrotic cell death evaluated by lactate dehydrogenase activity assay. The K(v)7 blocker linopirdine increased OGD-evoked dopamine efflux and OGD-induced damage, and attenuated the effects of retigabine. Quantitative-PCR experiments showed that OGD caused an similar to 6-fold decrease in K(v)7.2 transcript, while levels of mRNAs encoding for other K(v)7 subunits were unaffected; western blot experiments showed a parallel reduction in K(v)7.2 protein levels. Retigabine also decreased the peak level of dopamine efflux induced by L-glutamate, and attenuated the loss of TTC staining induced by the excitotoxin. These results suggest a role for K(v)7.2 in modulating ischemia-evoked caudate damage.
机译：缺血性中风会导致纹状体多巴胺外流，从而导致细胞死亡。由于K（v）7钾离子通道调节多巴胺的释放，我们研究了其药理学调制对多巴胺外排的影响，通过快速循环伏安法（FCV）和神经毒性，对Wistar大鼠尾脑脑片进行了氧和葡萄糖剥夺（OGD） 。 K（v）7激活剂瑞替加滨和ICA27243延迟了发作，并降低了OGD诱导的多巴胺外排的峰值水平。并且通过2,3,5-三苯基四唑氯化物（TTC）染色也可以降低OGD诱导的损伤。瑞替加滨还通过乳酸脱氢酶活性测定降低了OGD诱导的坏死细胞死亡。 K（v）7阻断剂利诺比尔丁增加OGD诱发的多巴胺外排和OGD诱导的损伤，并减弱瑞替加滨的作用。定量PCR实验表明，OGD导致K（v）7.2转录本下降了约6倍，而编码其他K（v）7亚基的mRNA的水平却没有受到影响。免疫印迹实验表明K（v）7.2蛋白水平平行降低。瑞替加滨还降低了由L-谷氨酸诱导的多巴胺外排的峰值水平，并减弱了由兴奋毒素诱导的TTC染色的损失。这些结果表明K（v）7.2在调节缺血引起的尾状核损伤中的作用。

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