Local changes in multiunit activity (MUA), tissue oxygen tension (PtO2), and extracellular potassium ion concentration ([K+]0) were recorded simultaneously using both oxygen-sensing and ion-sensing microelectrodes in the bullfrog optic tectum to evaluate relationships between neuronal excitation, changes in [K+]0, and oxidative metabolism. Visual stimulation elicited a brief multiunit discharge, which was accomplished by elevation of [K+]0, 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, hypoxide, or asphyxia) resulted in elevation of resting [K+]0, an increase in the magnitude of visually evoked rises in [K+]0, and slowing of the rates of K+ removal. Metabolic inhibition also blocked or diminished the transient decrease in PtO2 that normally accompanied neuronal excitation. The results indicate that potassium ion homeostasis in the amphibian central nervous system (CNS) is dependent, in part, on active reuptake of potassium involving Na-K-ATPase, and that the energy required for this process is provided through oxidative metabolism. Potassium ion homeostasis in the amphibian appears to be regulated by processes similar to those reported for mammals.
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