科研之友
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摘要
Glial cells are believed to play a major role in the regulation of the extracellular potassium concentration ([K+](o)), particularly when the [K+](o) is increased. Using ion-selective electrodes, we compared the [K+](o) changes in the dentate gyrus of urethane-anaesthetized adult rats in the presence of reactive astrocytes and after reduction of glial function. The regulation of [K+](o) in the dentate gyrus was determined by measuring the ceiling level of [K+](o) and the half-time of recovery of [K+](o) during and after seizures produced by 20 Hz trains of stimulation to the angular bundle. Reactive astrocytes were induced by repeated seizures and their presence was confirmed by a qualitative increase in glial fibrillary acidic protein (GFAP) and vimentin immunoreactivity. To inhibit glial function, fluorocitrate (FC), a reversible metabolic inhibitor, or alpha-aminoadipate (alpha-AA), an irreversible toxin, was injected into the dentate gyrus region, and the regulation of [K+](o) was monitored for 8 h or 2 days later, respectively. After alpha-aminoadipate, loss of astrocytes in the dentate gyrus was demonstrated by loss of staining for GFAP. In the presence of reactive astrocytes there was no significant change in the peak [K+](o) during seizures or the half-time of recovery of [K+](o) after seizures compared to control animals, alpha-Aminoadipate significantly slowed the rate of recovery of [K+](o), but did not change the ceiling [K+](o). Fluorocitrate reversibly decreased the ceiling [K+](o), but also slowed the rate of recovery of [K+](o). Overall our results suggest that normal glial function is required for the recovery of elevated [K+](o) after seizures in vivo.
