Abstract
Acute or chronic administration of lithium chloride increased the disappearance of intracisternally administered norepinephrine-H3 from rat brain. Tritiated deaminated catechol metabolites and free deaminated-O-methylated metabolites represented a larger fraction of the radioactivity present in the brain in animals treated with lithium chloride than in control animals. Statistically significant changes in the uptake of norepinephrine-H3 into brain were not observed after the chronic administration of lithium chloride. The findings suggest that chronic, as well as acute administration of lithium salts may increase norepinephrine turnover in brain and possibly increase the deamination of this amine.
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