Brain (Na+, K+)‐ATPase and Noradrenergic Activity: Effects of Hyperinnervation and Denervation on High‐Affinity Ouabain Binding

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Abstract
To examine the role of nerve‐specific (Na+, K+)‐ATPase in chronic changes in noradrenergic activity, we examined the effects of noradrenergic denervation and hyperinnervation on p‐nitrophenylphosphatase activity and on total and nerve‐specific ouabain binding. High‐affinity and erythrosin B‐sensitive binding were compared as measurements of nerve‐specific binding. Hyperinnervation and denervation was produced in cerebellum and cerebral cortex, respectively, by 6‐hydroxydopamine lesions of the dorsal noradrenergic bundle. Hyperinnervation increased, and denervation decreased, enzyme activity, high‐affinity ouabain inhibition, and erythrosin B‐sensitive ouabain binding. As (Nat+, K+)‐ATPase has a major role in the regulation of neural excitability and energy metabolism, and the ouabain binding site has been shown to have endogenous ligands, these changes in (Na+, K+)‐ATPase may be important in the long‐term regulation of neuron function by norepinephrine.