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Adrenergic nerve degeneration induced by condensation products of adrenaline and acetaldehyde

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Summary

Adult and new-born rats were treated with MA 3 or MA 4 (tetrahydroisoquinoline alkaloids resulting from the condensation of adrenaline with acetaldehyde) to investigate the action of these alkaloids on the adrenergic innervation.

The irides, right heart auricles and superior cervical ganglia of control and treated rats were processed for microscopy and spectrofluorimetrical determination of noradrenaline (NA).

Marked ultrastructural alterations of the adrenergic nerve terminals were observed in the irides and auricles of the treated adult and new-born rats. The superior cervical ganglia of the adult rats exhibited only minor ultrastructural alterations while those of the new-born animals presented anomalies even at the light microscopy level.

Absence of significant alterations of the NA content in treated adult rats is attributed to the accumulation of fluorescing alkaloid derivatives.

We conclude that MA 3 and MA 4 can induce selective degeneration of the adrenergic nerve terminals of the adult rats and of the whole adrenergic neurone of new-born rats. They are, in this respect, less potent than 6-OHDA.

As evidence has been put forward that these alkaloids may be formed in vivo during ethanol intoxication, our results may constitute a contribution to the understanding of some of the phenomena related to ethanol intoxication and/or the alcohol withdrawal syndrome.

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Part of the results was presented to the 6th International Congress of Pharmacology, Helsinki 1975 (Abstr. 1513) and to the 6th Annual Meeting of the Portuguese Pharmacological Society (Lisbon, 1976). This work was supported by a grant from Instituto Nacional de Investigação Científica (PMC-2)

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Azevedo, I., Osswald, W. & Vasques, M.L. Adrenergic nerve degeneration induced by condensation products of adrenaline and acetaldehyde. Naunyn-Schmiedeberg's Arch. Pharmacol. 300, 139–144 (1977). https://doi.org/10.1007/BF00505044

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