Abstract
The effects of drugs and metabolic inhibitors on the uptake, release and metabolism of intraventricularly administered H3-norepinephnine in the rat brain are described. Amphetamine, reserpine and guanethidine, but not cocaine, D-lysergic acid diethylamide, mescaline or bretylium, block the uptake or accumulation of H3-norepinephrine in the brain. Monoamine oxidase inhibition produces an elevation of H3-norepinephrine and H3-normetanephrine in the brain. A catechol O-methyl transferase inhibitor, tropolone-4-acetamide, reduces the level of H3-normetanephrine but has no effect on the level of H3-norepinephrine. Amphetamine and reserpine release H3-norepinephrine in a different manner. Amphetamine administration results in an elevation of normetanephrine levels, while reserpine administration causes an elevation of O-methylated deaminated metabolites. Both drugs release a greater proportion of the brain content of H3-norepinephrine when they are administered a long time after the injection of the radioactive catecholamine than after a short time. The different actions of amphetamine and reserpine on the metabolism of H3-norepinephrine indicate the presence of more than one storage form of the brain catecholamine.
Footnotes
- Accepted March 9, 1965.
- The Williams & Wilkins Comapny
JPET articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|