Sodium pump activity, not glial spatial buffering, clears potassium after epileptiform activity induced in the dentate gyrus.
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.
Xiong
Z Q
ZQ
Department of Pharmacology and Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
Stringer
J L
JL
D000818:Animals; D002712:Chlorides / Q000502:physiology; D018891:Dentate Gyrus / Q000187:drug effects / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004827:Epilepsy / Q000378:metabolism*; D005071:Evoked Potentials / Q000502:physiology; D005110:Extracellular Space / Q000378:metabolism; D017629:Gap Junctions / Q000187:drug effects; D066298:In Vitro Techniques; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D002712:Chlorides; D004791:Enzyme Inhibitors; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D013779:Tetrodotoxin; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium