Two-pore-domain potassium channels contribute to neuronal potassium release and glial potassium buffering in the rat hippocampus
Two-pore-domain potassium channels contribute to neuronal potassium release and glial potassium buffering in the rat hippocampus
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DOI：
10.1016/j.brainres.2007.07.013
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发表时间：
2007-10
期刊：
影响因子：
2.9
通讯作者：
Dennis Päsler;S. Gabriel;U. Heinemann
中科院分区：
文献类型：
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作者：
Dennis Päsler;S. Gabriel;U. Heinemann
双孔域钾离子（K2P）通道被认为参与神经元K+释放和胶质K+摄取。我们研究了K2P通道阻滞剂奎宁（200 μM或500 μM）、奎尼丁（500 μM）和布比卡因（200 μM）在AMPA/kainate和NMDA受体拮拮剂存在的情况下，对刺激诱导的大鼠海马CA1区细胞外钾浓度（[K+]o）的瞬时升高和离子离子诱导的瞬时升高的影响。重复肺泡刺激（20 Hz）引起的[K+]增加被奎宁和奎尼丁阻断，但种群峰值的幅度仅略有降低。布比卡因抑制了[K+]的上升和人口峰值。相比之下，奎宁和奎尼丁可适度增强离子导电诱导的[K+]升高，而布比卡因则没有作用。在有奎宁、奎尼丁和布比卡因存在的情况下，浓度为2mm的钡离子会阻断钾向内整流（Kir）和一些K2P通道，从而使[K+]增加。数据表明，奎宁/奎尼丁敏感的K2P通道介导神经元的K+释放，并可能有助于胶质细胞K+缓冲。
Two-pore-domain potassium (K2P) channels have been suggested to be involved in neuronal K+release and glial K+uptake. We studied effects of the K2P channel blockers quinine (200 or 500 μM), quinidine (500 μM), and bupivacaine (200 μM) on stimulus-induced and iontophoretically induced transient increases of the extracellular potassium concentration ([K+]o) in area CA1 of rat hippocampal slices, always in presence of AMPA/kainate and NMDA receptor antagonists. Increases in [K+]oevoked by repetitive alvear stimulation (20 Hz) were blocked by quinine and quinidine but amplitudes of population spikes were only modestly reduced. Bupivacaine suppressed both rises in [K+]oand population spikes. In contrast, iontophoretically induced rises in [K+]owere moderately augmented by quinine and quinidine while bupivacaine had no effect. Barium at concentrations of 2 mM which should block both potassium inward rectifier (Kir) and some K2P channels doubled iontophoretically induced rises in [K+]oalso in presence of quinine, quinidine, and bupivacaine. The data suggest that quinine/quinidine-sensitive K2P channels mediate K+release from neurons and possibly contribute to glial K+buffering.