Deletion of aquaporin-4 increases extracellular K(+) concentration during synaptic stimulation in mouse hippocampus.
Deletion of aquaporin-4 increases extracellular K(+) concentration during synaptic stimulation in mouse hippocampus.
复制标题
在小鼠海马中突触刺激期间，水通道蛋白4的缺失会增加细胞外K（+）浓度。
DOI：
10.1007/s00429-014-0767-z
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发表时间：
2015-07
影响因子：
3.1
通讯作者：
Nagelhus EA
中科院分区：
文献类型：
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作者：
Haj-Yasein NN;Bugge CE;Jensen V;Østby I;Ottersen OP;Hvalby Ø;Nagelhus EA
水通道水通道蛋白-4(AQP4)与K+转运之间的偶联引起了人们的极大兴趣。在这项研究中，我们评估了Aqp4缺失对活动诱导的成年小鼠海马区和穹隆体部急性脑片[K+]o变化的影响。我们发现，Aqp4缺失对[K+]o具有层特异性效应，这精确地反映了已知的对细胞外体积动力学的影响。在CA1区，Aqp4−/−小鼠在20 Hz刺激Schaffer侧支/连合纤维时辐射层的[K+]o峰值显著高于野生型，而在整个恢复期无明显差异。Aqp4基因缺失对锥体层和穹隆体区的[K+]o峰值和刺激后[K+]o恢复均无影响。我们的数据表明，在突触刺激过程中，AQP4通过对细胞外间隙体积的影响来调制[K+]o。
The coupling between the water channel aquaporin-4 (AQP4) and K+ transport has attracted much interest. In this study, we assessed the effect of Aqp4 deletion on activity-induced [K+]o changes in acute slices from hippocampus and corpus callosum of adult mice. We show that Aqp4 deletion has a layer-specific effect on [K+]o that precisely mirrors the known effect on extracellular volume dynamics. In CA1, the peak [K+]o in stratum radiatum during 20 Hz stimulation of Schaffer collateral/commissural fibers was significantly higher in Aqp4 −/− mice than in wild types, whereas no differences were observed throughout the [K+]o recovery phase. In stratum pyramidale and corpus callosum, neither peak [K+]o nor post-stimulus [K+]o recovery was affected by Aqp4 deletion. Our data suggest that AQP4 modulates [K+]o during synaptic stimulation through its effect on extracellular space volume.