The Impact of the Inward Rectifier Potassium Channels(kir4.1) in Astrocyte on Extracellular Potassium Buffering
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- 英文论文题名：The Impact of the Inward Rectifier Potassium Channels(kir4.1) in Astrocyte on Extracellular Potassium Buffering
- 论文作者：Mengmeng Du ; Wu Ying ; Li Jiajia
- 英文论文作者：Mengmeng Du ; Wu Ying ; Li Jiajia ; State Key Laboratory for Strength and Vibration of Mechanical Structures ; School of Aerospace ; Xi'an Jiaotong University
- 年：2016
- 作者机构：State Key Laboratory for Strength and Vibration of Mechanical Structures,School of Aerospace, Xi'an Jiaotong University;
- 英文论文关键词：potassium buffering ; Kir4.1 channels ; astrocyte
- 会议召开时间：2016-08-04
- 会议录名称：第三届全国神经动力学学术会议论文摘要集
- 语种：英文
- 分类号：R329.2
- 学会代码：AGLU
- 会议名称：第三届全国神经动力学学术会议
- 会议地点：中国甘肃敦煌
- 主办单位：中国力学学会动力学与控制专业委员会神经动力学专业组
- 学会名称：中国力学学会
- 页数：1
- 文件大小：611k
- 原文格式：D
- 会议级别：全国
摘要
Previous studies and experiments have been showed that elevated K+concentration in the extracellular space can induce pathological discharge activities,such as epilepsy[1].The inward rectifier potassium channels(Kir4.1)in brain astrocytes is crucial for the maintenance of the extracellular potassium buffering[2].Therefore,studying the relations between kir4.1 channels and discharge activities through theoretical analysis methods will provide a strong guidance for understanding normal activities of the brain and treating epilepsy.This paper simulates the effect of the kir4.1 channels blocker by setting the kir4.1 current is equal to zero approximately.Our model reproduces several phenomena observed experimentally:Firstly,in contrast to control condition,long-lasting stimulation will induce the pronounced undershoot of the extracellular potassium concentration.Moreover,we found that K+concentration in the extracellular space takes longer period to return to baseline after stimulation as kir4.1 channels is blocked.Furthermore,K+concentration baseline in astrocyte is higher and it rises more slowly to a lower peak value compared with control condition.These results are all in good qualitative agreement with the experiments of[3;4].In addition,our results confirm the vital role of kir4.1 channels for extracellular potassium buffering by glia.
Previous studies and experiments have been showed that elevated K+ concentration in the extracellular space can induce pathological discharge activities, such as epilepsy [1]. The inward rectifier potassium channels(Kir4.1) in brain astrocytes is crucial for the maintenance of the extracellular potassium buffering[2]. Therefore, studying the relations between kir4.1 channels and discharge activities through theoretical analysis methods will provide a strong guidance for understanding normal activities of the brain and treating epilepsy. This paper simulates the effect of the kir4.1 channels blocker by setting the kir4.1 current is equal to zero approximately. Our model reproduces several phenomena observed experimentally: Firstly, in contrast to control condition,long-lasting stimulation will induce the pronounced undershoot of the extracellular potassium concentration. Moreover, we found that K+ concentration in the extracellular space takes longer period to return to baseline after stimulation as kir4.1 channels is blocked. Furthermore, K+ concentration baseline in astrocyte is higher and it rises more slowly to a lower peak value compared with control condition. These results are all in good qualitative agreement with the experiments of [3; 4]. In addition, our results confirm the vital role of kir4.1 channels for extracellular potassium buffering by glia.
Previous studies and experiments have been showed that elevated K+ concentration in the extracellular space can induce pathological discharge activities, such as epilepsy [1]. The inward rectifier potassium channels(Kir4.1) in brain astrocytes is crucial for the maintenance of the extracellular potassium buffering[2]. Therefore, studying the relations between kir4.1 channels and discharge activities through theoretical analysis methods will provide a strong guidance for understanding normal activities of the brain and treating epilepsy. This paper simulates the effect of the kir4.1 channels blocker by setting the kir4.1 current is equal to zero approximately. Our model reproduces several phenomena observed experimentally: Firstly, in contrast to control condition,long-lasting stimulation will induce the pronounced undershoot of the extracellular potassium concentration. Moreover, we found that K+ concentration in the extracellular space takes longer period to return to baseline after stimulation as kir4.1 channels is blocked. Furthermore, K+ concentration baseline in astrocyte is higher and it rises more slowly to a lower peak value compared with control condition. These results are all in good qualitative agreement with the experiments of [3; 4]. In addition, our results confirm the vital role of kir4.1 channels for extracellular potassium buffering by glia.
引文
[1]Traynelis S F,Dingledine R.Potassium-induced spontaneous electrographic seizures in the rat hippocampal slice[J].Journal of Neurophysiology,1988,59(1):259-76.
[2]Nagao Y,Harada Y,Mukai T,et al.Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model.[J].Frontiers in Cellular Neuroscience,2013,7(28):104.
[3]Witthoft A,Filosa J,Karniadakis G E.Potassium buffering in the neurovascular unit:models and sensitivity analysis.[J].Biophysical Journal,2013,105(9):2046-54.
[4]Chever O,Djukic B,Mccarthy K D,et al.Implication of K(ir)4.1 Channel in Excess Potassium Clearance:An In Vivo Study on Anesthetized Glial-Conditional K(ir)4.1 Knock-Out Mice[J].Journal of Neuroscience the Official Journal of the Society for Neuroscience,2010,30(47):15769-15777.
[2]Nagao Y,Harada Y,Mukai T,et al.Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model.[J].Frontiers in Cellular Neuroscience,2013,7(28):104.
[3]Witthoft A,Filosa J,Karniadakis G E.Potassium buffering in the neurovascular unit:models and sensitivity analysis.[J].Biophysical Journal,2013,105(9):2046-54.
[4]Chever O,Djukic B,Mccarthy K D,et al.Implication of K(ir)4.1 Channel in Excess Potassium Clearance:An In Vivo Study on Anesthetized Glial-Conditional K(ir)4.1 Knock-Out Mice[J].Journal of Neuroscience the Official Journal of the Society for Neuroscience,2010,30(47):15769-15777.