Outward chloride/cation co-transport in mammalian cortical neurons.
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.
Thompson
S M
SM
Department of Neurology, Stanford University, School of Medicine, CA 94305.
Deisz
R A
RA
Prince
D A
DA
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002034:Bumetanide / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D002712:Chlorides / Q000493:pharmacokinetics* / Q000502:physiology; D004558:Electric Stimulation; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009433:Neural Inhibition / Q000187:drug effects; D013449:Sulfonamides / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002712:Chlorides; D013449:Sulfonamides; D002034:Bumetanide; D005680:gamma-Aminobutyric Acid; C015451:piretanide