The effect of nerve lesions on the inflammatory response to injury

Helme, R. D.; Andrews, Paul V.

doi:10.1002/jnr.490130311

Cited by 50 publications

(21 citation statements)

References 13 publications

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“…For example, sympathetic nerve stimulation increases vascular permeability, even though it also produces vasoconstriction (5). Consistent with these data, surgical (6, 7) or chemical (8)(9)(10) sympathectomy strongly inhibits noxious stimulus-evoked plasma extravasation (PE), a major sign of acute inflammation. Sympathectomy also markedly reduces inflammation and joint injury in rats with adjuvant-induced arthritis (11).…”

supporting

confidence: 62%

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Green

Basbaum

Helms

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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We assessed the contribution of ATP and adenosine (i) to a major sign of acute inflammation, plasma extravasation (PE), in the rat knee joint and (ii) to the severity of joint injury in adjuvant-induced experimental arthritis, a chronic inflammatory disease. PE induced by local infusion of bradykinin, which we have previously shown to depend on the sympathetic postganglionic neuron terminal, was markedly enhanced by coinfusion of either ATP or the adenosine A2-receptor agonist 2-[4-(2-carboxyethyl)phenylethylaminoJ-5'-Nethylcarboxamidoadenosine. Bradykinin-induced PE was inhibited by coinfusion of the ATP receptor antagonist adenosine 5'-[a,4-methyleneltripbosphate, the A2-receptor antagonist 3-(5H-thiozolo[2,3b]quinazolin-3-yl)phenol monohydrochloride, or the adenosine Al-receptor agonist N6-cyclopentyladenosine. The joint injury associated with experimental arthritis, which is reduced in severity in sympathectomized rats, was also markedly attenuated by daily administration of either ATP (40% reduction) or adenosine (55% reduction). These results demonstrate that the purines ATP and adenosine (acting at the A2 receptor), cotransmitters in the sympathetic postganglionic neuron terminal, enhance bradykinin-induced sympathetic postganglionic neuron terminal-dependent PE but inhibit the joint injury of arthritis. These opposing purinergic effects on PE and joint hijury suggest that enhanced PE protects against joint iury.A contribution of the peripheral limb of the sympathetic nervous system to inflammation has been demonstrated in a variety of animal models (1,2) and also in patients with inflammatory diseases, such as rheumatoid arthritis (3, 4). For example, sympathetic nerve stimulation increases vascular permeability, even though it also produces vasoconstriction (5). Consistent with these data, surgical (6, 7) or chemical (8-10) sympathectomy strongly inhibits noxious stimulus-evoked plasma extravasation (PE), a major sign of acute inflammation. Sympathectomy also markedly reduces inflammation and joint injury in rats with adjuvant-induced arthritis (11).We have recently shown that the PE produced by bradykinin (BK), a potent inflammatory agent, is mediated via an action on the sympathetic postganglionic neuron (SPGN) terminal (12). Specifically, sympathectomy significantly reduced PE evoked by infusion of BK into the knee joint of the rat. Although many SPGN neurotransmitters have been identified, our results suggested that release of the known sympathetic "cotransmitters" (i.e., norepinephrine, neuropeptide Y, and ATP) could not alone account for the PE produced by SPGN-terminal stimulation. Thus, norepinephrine inhibited PE, and neuropeptide Y had no effect on PE.Although ATP increased-PE, its effect, even at the highest doses, was smaller in amplitude and much shorter in duration than that produced by BK or by acute activation of SPGN terminals with 6-hydroxydopamine (12). Because indomethacin, a prostaglandin synthesis inhibitor, markedly reduced the PE produced by BK and because SPGNs synthesiz...

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supporting

confidence: 62%

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Green

Basbaum

Helms

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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“…CGRP and SP, released during tissue damage, produce vasodilation and plasma extravasation (Brain et al, 1992;Brain and Williams, 1989;Lembeck and Holzer, 1979;Saria, 1984), which, in turn, allow the infiltration of additional inflammatory mediators (Bar-Shavit et al, 1980;Hartung et al, 1986;Helme and Andrews, 1985;Payan et al, 1984;Saito et al, 1986). Peptide release also activates mast cells to release histamine (Johnson and Erdos, 1973;.…”

Section: Functional Roles For the H 3 Rmentioning

confidence: 99%

Immunohistochemical localization of histamine H3 receptors in rodent skin, dorsal root ganglia, superior cervical ganglia, and spinal cord: Potential antinociceptive targets

Cannon

Chazot

Hann

et al. 2007

Pain

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Activation of histamine H 3 receptors (H 3 Rs) reduces inflammation and nociception, but the existence of H 3 Rs on peripheral innervation has never been demonstrated. Here we use antibodies to locate H 3 Rs in whisker pads, hairy and glabrous hind paw skin, dorsal root ganglia (DRGs), and spinal cords of rats, wild-type mice, and H 3 R knockout (H 3 KO) mice. Although H 3 Rs have been hypothesized to be on C and sympathetic fibers, H 3 R-like immunoreactivity (H 3 R-LI) was only detected on presumptive periarterial Aδ fibers and on Aβ fibers that terminated in Meissner's corpuscles and as lanceolate endings around hair follicles. The H 3 R-positive periarterial fibers were thin-caliber and coexpressed immunoreactivity for calcitonin gene-related peptide (CGRP), substance P, acid sensing ion channel 3 and 200kD neurofilament protein (NF). H 3 R-LI was also detected on epidermal keratinocytes and Merkel cells, but not on Merkel endings, C fibers, any other Aδ fibers, or sympathetic fibers. In DRGs, H 3 R-LI was preponderantly on medium to large neurons coexpressing NF-LI and mostly CGRP-LI. In dorsal horn, CGRP-positive fibers with and without H 3 R-LI ramified extensively in lamina II; many of the former formed a plexus in lamina V. Low levels of H 3 R-LI were also present on Aβ fibers penetrating superficial and into deeper laminae. The distribution of H 3 R-LI was similar in rats and wild-type mice, but was eliminated or strongly reduced in Aδ fibers and Aβ fibers, respectively, in H 3 KO mice. Taken with recently published behavioral results, the present findings suggest that periarterial, peptidergic, H 3 R-containing Aδ fibers may be sources of high threshold mechanical nociception.

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“…with no au tonomic denervation) reduced the inflam matory reaction to heating or to streptococ cal infection. Treatment of rats with capsai cin produces a highly selective loss of many nociceptive C-fibres, but no loss of auto nomic fibres or reduction in autonomic re- sponses [21,[24][25][26], Following such treat ment a number of inflammatory reactions are reduced, such as oedema following skin heating [27], adjuvant arthritis [28,29] and white cell numbers in skin blisters induced by freezing [30], There is, therefore, plenty of evidence for a neurogenic component in a wide variety of inflammatory models. Even where the ef fects of denervation are small, this does not mean that neurogenic factors are insignifi cant.…”

Section: Significance Of the Neurogenic Component For Inflammation Inmentioning

confidence: 99%

Neurogenic Inflammation

Lynn¹

1988

Skin Pharmacol Physiol

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The main elements of neurogenic inflammation in the skin – antidromic vasodilatation, axon reflex flare and neurogenic plasma extravasation – are briefly described. New evidence is presented for a contribution from small myelinated fibres, as well as unmyelinated fibres, to antidromic vasodilatation. The mechanisms underlying flare are discussed and it is argued that weak coupling between C-fibre terminals must be important in determining the extent of spread of vasodilatation. The extent to which neurogenic factors contribute to a range of inflammatory models and to inflammatory disease states is discussed; it is argued that the importance of neurogenic mechanisms may have been underestimated.

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The effect of nerve lesions on the inflammatory response to injury

Cited by 50 publications

References 13 publications

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Immunohistochemical localization of histamine H3 receptors in rodent skin, dorsal root ganglia, superior cervical ganglia, and spinal cord: Potential antinociceptive targets

Neurogenic Inflammation

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