Haemodynamic and immunohistochemical studies of rat incisor pulp after denervation and subsequent re-innervation.
The effects of injury to the inferior alveolar nerve on the distribution of neuropeptides and neurogenic blood-flow reactions were studied in rat mandibular dental pulp. In normal incisor pulps, calcitonin gene-related peptide (CGRP)-like immunoreactivity was common, while substance P- and neurokinin (NKA)-positive nerve fibres were much less abundant. There were no signs of vasoactive intestinal peptide-like, neuropeptide Y-like or 5-hydroxytryptamine-like immunoreactivity. In normal pulps, electrical stimulation (100 microA, 5 ms, 15 Hz for 30 s) of the tooth crown resulted in transient vasoconstriction followed by vasodilation, which was enhanced after alpha-adrenoceptor blockade. At 3 days-4 weeks after unilateral nerve section there were no signs of CGRP-, substance P- and NKA-immunoreactivity, and there was no vasodilation in response to tooth stimulation. The vasoconstrictor response was also absent during this period but at 4 weeks postoperatively a weak response was obtained and after 7 weeks the vasoconstrictor response had regained normal amplitude. At 7 weeks postoperatively, a large number of CGRP-positive fibres had reappeared and at 11 weeks the pattern of CGRP-immunoreactivity was normal. However, substance P- and NKA-immunoreactivity were not found at 7 or 11 weeks after surgery. Vasodilator responses appeared at 7 weeks, and showed normal amplitude at 11 weeks after the creation of the nerve lesion. The results show that during nerve regeneration, sympathetic vasoconstriction was regained earlier than neurogenic vasodilation in rat incisor teeth. The reappearance of neurogenic vasodilation after nerve injury was temporarily associated with the presence of CGRP-immunoreactivity in regenerating trigeminal afferent nerves.
Kerezoudis
N P
NP
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Fried
K
K
Olgart
L
L
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D003714:Denervation; D003782:Dental Pulp / Q000098:blood supply / Q000294:innervation* / Q000378:metabolism; D004558:Electric Stimulation; D006439:Hemodynamics; D007150:Immunohistochemistry; D007180:Incisor; D008297:Male; D008340:Mandibular Nerve / Q000098:blood supply / Q000378:metabolism / Q000502:physiology* / Q000601:surgery; D009412:Nerve Fibers / Q000648:ultrastructure; D009416:Nerve Regeneration; D015288:Neurokinin A / Q000378:metabolism; D009475:Neurons, Afferent / Q000378:metabolism / Q000648:ultrastructure; D009478:Neuropeptide Y / Q000378:metabolism; D009479:Neuropeptides / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D012701:Serotonin / Q000378:metabolism; D013373:Substance P / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000033:anatomy & histology / Q000378:metabolism; D014276:Trigeminal Nerve / Q000033:anatomy & histology / Q000378:metabolism; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism; D014661:Vasoconstriction; D014664:Vasodilation
D000317:Adrenergic alpha-Antagonists; D009478:Neuropeptide Y; D009479:Neuropeptides; D012701:Serotonin; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D015288:Neurokinin A; D015740:Calcitonin Gene-Related Peptide