Effects of 6-Hydroxydopamine on Noradrenaline-containing Neurones in the Rat Brain

Abstract

THE compound 6-hydroxydopamine (2,4,5-trihydroxyphenylethylamine) produces a long lasting depletion of noradrenaline (NA) from peripheral sympathetically innervated tissues in various species^1,2. It was originally suggested that the depletion of noradrenaline produced by 6-hydroxydopamine might be a result of damage to the amine storage sites in sympathetic nerves in a manner similar to that of reserpine, or that, alternatively, 6-hydroxydopamine might act as a “false transmitter” and displace noradrenaline from sympathetic nerves^1–4. Electron microscopy has shown recently, however, that after treatment with 6-hydroxydopamine the terminal regions of peripheral adrenergic nerves degenerate and eventually disappear⁵. The noradrenaline depletion produced by 6-hydroxydopamine has been suggested to result from this acute degeneration of adrenergic terminals. This hypothesis was supported by the histochemical evidence that after treatment with 6-hydroxydopamine the fluorescent network of sympathetic nerve terminals in the rat iris disappeared, while the fluorescence of preterminal axons increased⁶. 6-Hydroxydopamine thus induces changes similar to those seen after section of an adrenergic nerve, suggesting that this compound produces a “chemical sympathectomy”⁵.