After a single i.v. injection, 6-OHDOPA is capable of causing destruction and/or functional impairment of noradrenergic nerve terminals in both the central and the peripheral nervous system. By analogy with the effects of 6-hydroxydopamine and histochemical observations of preterminal accumulation of neurotransmitters, the conclusion that 6-OHDOPA causes degenerative changes in the terminal plexus is derived. There is no question that the final determination of neuronal degeneration should come from electron microscopic studies. The accumulation of histochemically observable catecholamine fluorescence in nonterminal axons, the time course of depletion and recovery of NE within various peripheral organs and impairment of uptake of exogenously administered NE support the conclusion that 6-OHDOPA has the potential to cause selective destruction of noradrenergic terminals. 6-OHDOPA is a valuable tool for the investigation of central pathways and functional organization of the noradrenergic neurons in the brain. Injection of 6-OHDOPA into the cerebral ventricles can produce a highly specific reduction in the NE content of the central nervous system while leaving dopaminergic neurons unaffected. This factor will be useful for the exploration of the behavioral contributions of central noradrenergic neurons.
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