Degeneration and regeneration of adrenergic nerves in mesenteric blood vessels, iris and atrium of the rat after 6-hydroxydopamine injection.
Degeneration of adrenergic axons after 6-hydroxydopamine (6-OH-DA), 2 times 68 mg kg-1 i.v. within 6h, and the subsequent regeneration process over the following 205 days were studied in rat mesenteric vessels, wight atria and irides, using the histochemical fluorescence method of Falck and Hillarp. The objective of the study was to determine why noradrenaline is less depleted and recovers much more rapidly in the mesentery than in other tissues after 6-OH-DA (Finch et al., 1973). The mesentery was further studied by electron microscopy and noradrenaline content analyses, until day 29 after 6-OH-DA treatment. Virtually all adrenergic terminal axons in these tissues were destroyed one day after 6-OH-DA. The large nonterminal axon bundles which occur along the mesenteric vessels and rarely in the heart survived and revealed an intensified catecholamine fluorescence; correspondingly, the mesenteric noradrenaline content was only reduced to 29% of control values. In contrast, such large nonterminal axon bundles were not observed in control iris preparations, and no adrenergic fibres survived in the irides, as suggested by fluorescence microscopy. Regenerating axons were observed in all organs after 3-8 days. The number of nerve terminals along the circumference of the external elastic lamina, as observed in ultrathin cross sections of mesenteric vessels, appeared virtually normal 4 weeks after treatment. Meanwhile, the noradrenaline content of the mesentery returned to approximately 85% of control values. As suggested by fluorescence microscopy, complete adrenergic regeneration occurred in mesenteric vessels between days 46 and 105, while regeneration in atrium and iris was incomplete even at day 205; The density of adrenergic axons in the iris, morphometrically determined, was only 76% and 88% of controls on days 160 and 205, respectively. The survival of the many large nonterminal axon bundles in the mesentery with increased NA content explains the relatively small NA depletion of the mesentery; The rapid recovery of the mesenteric NA content is due to faster regeneration of adrenergic terminal axons in the mesentery as compared with iris and atrium. This is tentatively explained in terms of sprouting from the large axon bundles surviving close to the destroyed terminal axons of the mesenteric vessels, whereas in the other tissues no (iris) or only a few (atrium) large nonterminal axon bundles occur and persist to act as a source of quickly regenerated terminal axons.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D006321:Heart / Q000294:innervation*; D006325:Heart Atria; D006651:Histocytochemistry; D006892:Hydroxydopamines / Q000494:pharmacology*; D007498:Iris / Q000294:innervation*; D008297:Male; D008638:Mesenteric Arteries / Q000294:innervation*; D008642:Mesenteric Veins / Q000294:innervation*; D008856:Microscopy, Fluorescence; D009410:Nerve Degeneration / Q000187:drug effects*; D009416:Nerve Regeneration / Q000187:drug effects*; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D012583:Schwann Cells / Q000648:ultrastructure; D013564:Sympathetic Nervous System / Q000378:metabolism* / Q000648:ultrastructure; D013997:Time Factors
D006892:Hydroxydopamines; D009638:Norepinephrine