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The frog retrolingual membrane was used as a model microcirculatory system for evaluating the role of neural control. Terminal arterioles were studied before and 2 to 21 days after topical application of 6-hydroxydopamine (6-HDA). When arterioles were visualized microscopically in vivo and stimulated directly with a microelectrode, 6-HDA reduced the normal, longitudinally conducted vasoconstriction to a local response. Current intensities needed for threshold responses averaged more than fourfold those of control thresholds. Nerve induced vasoconstriction was abolished, whereas nerve-induced vasodilation persisted after 6-HDA. Ultrastructurally, 6-HDA produced extensive degeneration only in perivascular nerves containing large granular vesicles, although vasomotor nerves with clear vesicles, vascular smooth muscle, Schwann cells, endothelial cells, motor end plates, and striated muscle appeared normal after 6-HDA treatment. Autoradiography and fluorescence histochemistry revealed that the perivascular nerves were no longer capable of taking up or binding exogenous catecholamine. The results indicate that topically applied 6-HDA produces selective dysfunction of adrenergic nerves correlated with fine structural degeneration. The absence of conducted vasoconstrictor responses in this preparation indicates their dependence on an intact adrenergic nerve supply.

Cytochemical and Physiological Effects of 6-Hydroxydopamine on Periarteriolar Nerves of Frogs