The Journal of Neurophysiology Vol. 83 No. 3 March 2000, pp. 1443-1451
Copyright ©2000 by the American Physiological Society

Sodium Pump Activity, Not Glial Spatial Buffering, Clears Potassium After Epileptiform Activity Induced in the Dentate Gyrus

Department of Pharmacology and Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030

Xiong, Zhi-Qi and Janet L. Stringer. Sodium Pump Activity, Not Glial Spatial Buffering, Clears Potassium After Epileptiform Activity Induced in the Dentate Gyrus. J. Neurophysiol. 83: 1443-1451, 2000. A number of mechanisms have been proposed to play a role in the regulation of activity-dependent variations in extracellular potassium concentration ([K⁺]_o). We tested possible regulatory mechanisms for [K⁺]_o during spontaneous recurrent epileptiform activity induced in the dentate gyrus of hippocampal slices from adult rats by perfusion with 8 mM potassium and 0-added calcium medium in an interface chamber. Local application of tetrodotoxin blocked local [K⁺]_o changes, suggesting that potassium is released and taken up locally. Perfusion with barium or cesium, blockers of the inward rectifying potassium channel, did not alter the baseline [K⁺]_o, the ceiling level of [K⁺]_o reached during the burst, or the rate of [K⁺]_o recovery after termination of the bursts. Decreasing gap junctional conductance did not change the baseline [K⁺]_o or the half-time of recovery of the [K⁺]_o after the bursts but did cause a decrease in the ceiling level of [K⁺]_o. Perfusion with furosemide, which will block cation/chloride cotransporters, or perfusion with low chloride did not change the baseline [K⁺]_o or the half-time of recovery of the [K⁺]_o after the bursts but did increase the ceiling level of [K⁺]_o. Bath or local application of ouabain, a Na⁺/K⁺-ATPase inhibitor, increased the baseline [K⁺]_o, slowed the rate of [K⁺]_o recovery, and induced spreading depression. These findings suggest that potassium redistribution by glia only plays a minor role in the regulation of [K⁺]_o in this model. The major regulator of [K⁺]_o in this model appears to be uptake via a Na⁺/K⁺-ATPase, most likely neuronal.