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GIRK通道开放剂在癫痫大鼠中抗癫痫的研究 被引量:1
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作者 吕华军 钟国栋 《中国现代医生》 2013年第16期10-11,15,共3页
目的探讨GIRK通道开放剂氟吡汀(flupirtine)对癫痫大鼠癫痫发作和脑电图的影响。方法 30只雄性健康成年SD大鼠随机平均分成三组:正常对照组、癫痫+生理盐水(NS)组和癫痫+氟吡汀(flupirtine)组。癫痫+生理盐水(NS)组和癫痫+氟吡汀(flupir... 目的探讨GIRK通道开放剂氟吡汀(flupirtine)对癫痫大鼠癫痫发作和脑电图的影响。方法 30只雄性健康成年SD大鼠随机平均分成三组:正常对照组、癫痫+生理盐水(NS)组和癫痫+氟吡汀(flupirtine)组。癫痫+生理盐水(NS)组和癫痫+氟吡汀(flupirtine)组两组动物复制青霉素诱发癫痫模型,造模成功后分别给予生理盐水和氟吡汀治疗,再观察痫样行为和脑电图。结果正常对照组行为学和脑电图均正常;癫痫+生理盐水组有明显痫样行为,脑电图呈现明显的尖波、棘波、尖-慢复合波以及棘-慢复合波的阵发性痫样放电;癫痫+氟吡汀组大部分大鼠行为正常或是轻度的痫样行为,脑电图恢复正常的基础波放电,只有1例呈少量的痫样放电。结论 GIRK通道开放剂flupirtine对癫痫大鼠痫样行为和异常的脑电图有改善作用。 展开更多
关键词 癫痫 girk通道 氟吡汀 大鼠
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碘化N-正丁基氟哌啶醇对豚鼠心房肌细胞乙酰胆碱敏感性钾通道的影响 被引量:5
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作者 刘冰 石刚刚 +1 位作者 高分飞 Lutz Pott 《中国药理学通报》 CAS CSCD 北大核心 2005年第5期544-550,共7页
目的研究碘化N正丁基氟哌啶醇(F2)对豚鼠心房肌细胞乙酰胆碱敏感性钾通道(KACh)的影响,探讨其对KACh的作用机制。方法采用膜片钳全细胞记录方法,测定F2对原代培养的豚鼠心房肌细胞乙酰胆碱敏感性钾电流IK(ACh)的影响。结果细胞外给予F2... 目的研究碘化N正丁基氟哌啶醇(F2)对豚鼠心房肌细胞乙酰胆碱敏感性钾通道(KACh)的影响,探讨其对KACh的作用机制。方法采用膜片钳全细胞记录方法,测定F2对原代培养的豚鼠心房肌细胞乙酰胆碱敏感性钾电流IK(ACh)的影响。结果细胞外给予F2对豚鼠心房肌细胞IK(ACh)呈可逆性、浓度依赖性的阻断作用。细胞内添入抗水解的GTP类似物GTPγS后,结果同前。细胞内给予50μmol·L-1F2对IK(ACh)无作用。结论F2是豚鼠心房肌细胞KACh的一种快速通道阻断剂,发挥作用部位在细胞膜外侧,作用位点在钾通道本身,与乙酰胆碱受体无关。 展开更多
关键词 碘化N-正丁基氟哌啶醇 心房肌细胞 乙酰胆碱敏感性钾通道(KACh) 膜片钳全细胞记录 G蛋白激活钾通道
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蛋白偶联内向整流钾通道的研究进展
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作者 王煜 杨晓苏 +1 位作者 龙小艳 肖波 《中国神经科学杂志》 CSCD 2003年第3期201-204,共4页
G蛋白偶联内向整流钾通道 (GIRK)是内向整流钾通道中的一个亚家族 ,由 5个亚单元GIRK 1~ 5组成。它能调节心率及神经细胞兴奋性和静息电位的水平 ,起慢突触后抑制作用。本文主要阐述GIRK在基因结构、分布、调控和病理生理方面的研究进展。
关键词 蛋白偶联 内向整流钾通道 基因结构 中枢神经系统 病理生理学
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Highlights for the 6th International Ion Channel Conference:ion channel structure,function,disease and therapeutics 被引量:3
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作者 Limei Wang Kewei Wang 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2017年第6期665-669,共5页
To foster communication and interactions amongst international scholars and scientists in the field of ion channel research, the 6 th International Ion Channel Conference(IICC-2017) was held between June 23–27, 2017 ... To foster communication and interactions amongst international scholars and scientists in the field of ion channel research, the 6 th International Ion Channel Conference(IICC-2017) was held between June 23–27, 2017 in the eastern coastal city of Qingdao, China. The meeting consisted of 450 attendees and 130 speakers and poster presenters. The program consisted of research progress, new findings and ongoing studies that were focused on(1) Ion channel structure and function;(2) Ion channel physiology and human diseases;(3) Ion channels as targets for drug discovery;(4) Technological advances in ion channel research. An insightful overview was presented on the structure and function of the mechanotransduction channel Drosophila NOMPC(No mechanoreceptor potential C), a member of the transient receptor potential(TRP) channel family. Recent studies on Transmembrane protein 16 or Anoctamin-1(TMEM16A, a member of the calcium-activated chloride channel [CaCC] family) were summarized as well. In addition, topics for ion channel regulation, homeostatic feedback and brain disorders were thoroughly discussed. The presentations at the IICC-2017 offer new insights into our understanding of ion channel structures and functions, and ion channels as targets for drug discovery. 展开更多
关键词 Ion channel STRUCTURE FUNCTION channelOPATHY Drug target MECHANOTRANSDUCTION Voltage-gated Ca2+ channel Anoctamin-1 Calcium activated chloride channel M-type potassium channel girk channel Voltage-gated sodium channel
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Characterization of Rebound Depolarization in Neurons of the Rat Medial Geniculate Body In Vitro 被引量:2
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作者 Xin-Xing Wang Yan Jin +4 位作者 Hui Sun Chunlei Ma Jinsheng Zhang Ming Wang Lin Chen 《Neuroscience Bulletin》 SCIE CAS CSCD 2016年第1期16-26,共11页
Rebound depolarization (RD) is a response to the offset from hyperpolarization of the neuronal mem- brane potential and is an important mechanism for the synaptic processing of inhibitory signals. In the present stu... Rebound depolarization (RD) is a response to the offset from hyperpolarization of the neuronal mem- brane potential and is an important mechanism for the synaptic processing of inhibitory signals. In the present study, we characterized RD in neurons of the rat medial geniculate body (MGB), a nucleus of the auditory thala- mus, using whole-cell patch-clamp and brain slices. RD was proportional in strength to the duration and magnitude of the hyperpolarization; was effectively blocked by Ni2+ or Mibefradil; and was depressed when the resting membrane potential was hyperpolarized by blocking hyperpolarization-activated cyclic nucleotide-gated (HCN) channels with ZD7288 or by activating G-protein-gated inwardly-rectifying K+ (GIRK) channels with baclofen. Our results demonstrated that RD in MGB neurons, which is carried by T-type Ca2+ channels, is critically regulated by HCN channels and likely by GIRK channels. 展开更多
关键词 Medial geniculate body Brain sliceRebound depolarizationchannel girk channel-type calcium channel - HCNResting membrane potential
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