RT Journal Article
SR Electronic
T1 THE EFFECT OF 6-HYDROXYDOPA ON PERIPHERAL ADRENERGIC NEURONS
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 284
OP 297
VO 183
IS 2
A1 RICHARD KOSTRZEWA
A1 DAVID JACOBOWITZ
YR 1972
UL http://jpet.aspetjournals.org/content/183/2/284.abstract
AB The time course of depletion and recovery of the norepinephrine (NE) content of several peripheral organs was studied after a single i.v. injection of 6-hydroxydopa (6-OHDOPA). The NE content of mouse cardiac ventricles, salivary glands, spleen and vas deferens was assayed and the adrenergic nerve plexus in various tissues was observed by the histochemical fluorescence method. 6-OHDOPA was capable of releasing NE from the ventricle, salivary glands and spleen in doses from 20 to 150 mg/kg i.v. The recovery of NE to control levels was complete in the salivary gland about two weeks after the 100 and 150 mg/kg doses, whereas the NE content of the ventricle did not return to control levels until three to six weeks after these dose levels. Perfusion of isolated hearts of 6-OHDOPA-treated rats with NE (1 µg/ml) for 10 minutes did not increase the number of adrenergic nerve terminals. A buildup of catecholamine fluorescence was observed in swollen preterminal axons of the rat iris. Pretreatment with a dopa decarboxylase inhibitor, L-α-hydrazine methyldopa (MK-486) or 3-hydroxy-4-bromobenzyloxyamine phosphate (NSD-1055) or D- or L-amphetamine, desipramine or chlorpromazine prevented the depleting effects of 6-OHDOPA in the ventricle. It is suggested that 6-OHDOPA is converted to 6-hydroxydopamine which is then capable of causing actual destruction of noradrenergic nerve terminals. © 1972 by The Williams & Wilkins Co.