Thompson S M, Deisz R A, Prince D A
Department of Neurology, Stanford University, School of Medicine, CA 94305.
Neurosci Lett. 1988 Jun 17;89(1):49-54. doi: 10.1016/0304-3940(88)90479-x.
The mechanism underlying outward chloride transport in guinea pig cingulate cortical neurons of in vitro slices was characterized with respect to its pharmacological antagonists and anion selectivity, and the nature of other ion movements coupled to Cl- transport. Changes in intracellular Cl- concentration, following iontophoresis of Cl- from KCl-filled intracellular recording electrodes, were estimated from changes in the amplitude of GABAergic, Cl(-)-mediated inhibitory postsynaptic potentials (IPSPs). The rate of outward Cl- transport was found to be reduced by bumetanide but not by SITS. SCN-, but not NO3-, was found to be actively transported. Increasing the extracellular K+ concentration ([K+]o) from 2.5 to 10 mM was found to inhibit Cl- extrusion. These data suggest that active Cl- extrusion from mammalian cortical neurons is mediated by an outwardly directed chloride/cation cotransport mechanism. Inhibition of this process by elevated [K+]o may be important in epilepsy.
通过其药理学拮抗剂和阴离子选择性，以及与Cl⁻转运相关的其他离子运动的性质，对豚鼠体外切片扣带皮层神经元中向外的氯离子转运机制进行了表征。从充满KCl的细胞内记录电极进行Cl⁻离子电泳后，细胞内Cl⁻浓度的变化是根据GABA能、Cl⁻介导的抑制性突触后电位（IPSP）幅度的变化来估计的。发现布美他尼可降低向外的Cl⁻转运速率，但SITS则无此作用。发现SCN⁻可被主动转运，而NO₃⁻则不能。将细胞外K⁺浓度（[K⁺]o）从2.5 mM提高到10 mM可抑制Cl⁻外流。这些数据表明，哺乳动物皮层神经元中的主动Cl⁻外流是由向外的氯化物/阳离子共转运机制介导的。升高的[K⁺]o对这一过程的抑制在癫痫中可能很重要。
