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6-Hydroxydopamine and Related Catecholaminergic Neurotoxins

Molecular Mechanisms

  • Chapter
Highly Selective Neurotoxins

Part of the book series: Contemporary Neuroscience ((CNEURO))

Abstract

6-Hydroxydopamine (6-HDA) (Fig. 1) first acquired neurochemical importance when it was reported as an in vivo metabolite of injected dopamine by Senoh et al. (1) Its peripheral noradrenergic depletion effects (2,3) were shown by Tranzer and Thoenen (4,5),using electron microscopy, to correspond to neuronal degeneration, and it was soon demonstrated to elicit neurodegeneration in noradrenergic and dopaminergic projections in the central nervous system (CNS) as well (6,7). Although immunosympathectomy (8) had preceded the appearance of 6-HDA by more than a decade as an alternative to simple surgical ablation in eliciting neurodegeneration, the broader applicability and considerable selectivity of 6-HDA quickly led to its extensive employment for such purposes. However, 6-HDA is not totally specific or complete in its degeneration of catecholaminergic neurons or associated projections even when employed under optimal conditions. The selectivity and potency of 6-HDA depend on the nature and age of the animal species, the environment of targeted neuronal entities, the dose, the manner of administration, and many other factors (9). The history, biological effects, selectivity, potency, biological significance, and clinical relevance of 6-HDA and its congeners have been extensively covered elsewhere (9–14),including Chapters 2–4. As such, we will only briefly mention such items in the current discussion.

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Blank, C.L., Lewis, R.J., Lehr, R.E. (1998). 6-Hydroxydopamine and Related Catecholaminergic Neurotoxins. In: Kostrzewa, R.M. (eds) Highly Selective Neurotoxins. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-477-1_1

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  • DOI: https://doi.org/10.1007/978-1-59259-477-1_1

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