Norepinephrine depletion alters cerebral oxidative metabolism in the "active" state.
Unilateral chemical lesion of the nucleus locus coeruleus in rats produced unilateral depletion of ipsilateral cortical norepinephrine. Norepinephrine depletion was not associated with changes in "resting" metabolic balance of the cerebral cortex, as determined by in situ reflection spectrophotometry of the redox state of cytochrome oxidase. Norepinephrine depletion, however, caused slowing of the transient metabolic response to sudden increases in energy demand produced by direct cortical electrical stimulation. The effect was apparent in the redox state of both cytochrome oxidase and NAD, the latter being measured, also in situ, by reflection microfluorometry. These results demonstrate that norepinephrine has a role in modulating the response to increased metabolic demand in the cerebral cortex. Norepinephrine may mediate its effect by potentiating Na+, K+-ATPase or through its effects on vascular reactivity, or both.
D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D003580:Cytochromes / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005071:Evoked Potentials; D007839:Functional Laterality; D006892:Hydroxydopamines / Q000494:pharmacology; D008125:Locus Coeruleus / Q000502:physiology; D008297:Male; D009243:NAD / Q000378:metabolism; D009638:Norepinephrine / Q000502:physiology*; D010084:Oxidation-Reduction; D010293:Pargyline / Q000494:pharmacology; D051381:Rats; D012039:Regional Blood Flow
D003580:Cytochromes; D006892:Hydroxydopamines; D009243:NAD; D010293:Pargyline; D003576:Electron Transport Complex IV; D009638:Norepinephrine