Potassium ion homeostasis in amphibian brain: contribution of active transport and oxidative metabolism.

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Abstract
Local changes in multiunit activity (MUA), tissue O2 tension (PtO2) and extracellular K+ concentration ([K+]O) were recorded simultaneously using both O2-sensing and ion-sensing microelectrodes in the bullfrog [Rana catesbeiana] optic tectum to evaluate relationships between neuronal excitation, changes in [K+]O, and oxidative metabolism. Visual stimulation elicited a brief multiunit discharge, which was accompanied by elevation of [K+]O, a negative DC potential shift, and a transient decrease in local tissue PtO2. The amplitude of these changes was related to the intensity of the multiunit discharge, which was varied by altering the position of the visual stimulus. Metabolic inhibition (ouabain, cyanide, hypoxia or asphyxia) resulted in elevation of resting [K+]O, an increase in the magnitude of visually evoked rises in [K+]O, and slowing of the rates of K+ removal. Metabolic inhibition also blocked or diminished the transient decrease in PtO2 that normally accompanied neuronal excitation. K+ homeostasis in the amphibian CNS is dependent, in part, on active reuptake of K+ involving Na-K-ATPase, and that the energy required for this process is provided through oxidative metabolism. K+ homeostasis in the amphibian appears to be regulated by processes similar to those reported for mammals.