Local oedema and general excitation of cutaneous sensory receptors produced by electrical stimulation of the saphenous nerve in the rat

Chahl, Loris A.; Ladd, Rachel

doi:10.1016/0304-3959(76)90043-9

Cited by 86 publications

(27 citation statements)

References 11 publications

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“…One observation that suggests it is an etiological factor is that whereas corticosteroids are effica- (14) (11,13,20,21). Capsaicin, the active ingredient in red peppers, is known to release SP/SK from the central and peripheral ends of these sensory nerves (2,12,20,21) and also appears to produce a set of responses in the GI tract of normal subjects similar to that seen in IBD patients. Thus, ingestion of capsaicin or a similar compound by a subject accustomed to bland food may elicit a crampy diarrhea, which although less severe, is similar to the symptoms presented in IBD patients.…”

Section: Resultsmentioning

confidence: 99%

Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease.

Mantyh

Gates

Zimmerman

et al. 1988

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

236

114

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Several lines of evidence indicate that tachykinin neuropeptides [substance P (SP), substance K (SK), and neuromedin K (NK)] play a role in regulating the inflammatory and immune responses. To test this hypothesis in a human inflammatory disease, quantitative receptor autoradiography was used to examine possible abnormalities in tachykinin binding sites in surgical specimens from patients with inflammatory bowel disease. Surgical specimens of colon were obtained from patients with ulcerative colitis (n = 4) and Crohn disease (n = 4). Normal tissue was obtained from uninvolved areas of extensive resections for carcinoma (n = 6). In all cases, specimens were obtained <5 min after removal to minimize influences associated with degradation artifacts and were processed for quantitative receptor autoradiography by using '2I-labeled Bolton-Hunter conjugates of NK, SK, and SP. In the normal colon a low concentration of SP receptor binding sites is expressed by submucosal arterioles and venules and a moderate concentration is expressed by the external circular muscle, whereas SK receptor binding sites are expressed in low concentrations by the external circular and longitudinal muscle. In contrast, specific NK binding sites were not observed in any area of the human colon. In colon tissue obtained from ulcerative colitis and Crohn disease patients, however, very high concentrations of SP receptor binding sites are expressed by arterioles and venules located in the submucosa, muscularis mucosa, external circular muscle, external longitudinal muscle, and serosa. In addition, very high concentrations of SP receptor binding sites are expressed within the germinal center of lymph nodules, whereas the concentrations of SP and SK binding sites expressed by the external muscle layers are not altered significantly. These results demonstrate that receptor binding sites for SP, but not SK or NK, are ectopically expressed in high concentrations (1000 -2000 times normal) by cells involved in mediating inflammatory and immune responses. These data suggest that SP may be involved in the pathophysiology of inflammatory bowel disease and might provide some insight into the interaction between the nervous system and the regulation of inflammation and the immune response in human inflammatory disease.identified within a subpopulation of these sensory neurons (1). The most extensively characterized of these sensory neuropeptides is substance P (SP), a member of the mammalian tachykinin family (Fig. 1), which also includes SK and NK. Though it is clear that SP and SK are expressed by sensory neurons (2) this remains uncertain for NK and derives from difficulty in generating highly specific antibodies for each of the tachykinins since they all share the highly antigenic carboxyl terminus -Phe-Xaa-Gly-Leu-Met-NH2,

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Section: Resultsmentioning

confidence: 99%

Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease.

Mantyh

Gates

Zimmerman

et al. 1988

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

236

114

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“…Inflammatory joint diseases such as rheumatoid arthritis often exhibit bilateral symmetry in the joints involved, and it is tempting to speculate that this could be mediated in part by blood-borne neuropeptides. These substances could act directly on the contralateral synovial vessels, or could induce inflammatory changes indirectly by activation ofcontralateral C fibres (Chahl & Ladd, 1976).…”

Section: Discussionmentioning

confidence: 99%

Extravasation in the knee induced by antidromic stimulation of articular C fibre afferents of the anaesthetized cat.

Ferrell¹,

Russell²

1986

The Journal of Physiology

112

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Electrical stimulation of the cut distal end of the posterior articular nerve (p.a.n.) of the cat knee joint resulted in significant extravasation of plasma proteins and erythrocytes into the synovial cavity of the knee. This effect was mediated by group IV afferents (C fibres) since stimulation of p.a.n. suprathreshold for group II or III afferents but subthreshold for group IV afferents did not produce extravasation. Unmyelinated sympathetic efferent fibres in the joint nerve did not contribute to the extravasation and were responsible for a diminution of this response as shown by the enhanced extravasation occurring after adrenergic blockade. Plasma and erythrocyte extravasation was mediated by afferents containing substance P (SP), as demonstrated by the reversible abolition of extravasation when the substance P antagonist (D‐Pro4,D‐Trp7,9,10)‐SP (4‐11) was injected into the synovial cavity. In some animals it was observed that electrical stimulation of the cut distal end of p.a.n. in one limb resulted in extravasation in the contralateral knee joint. It is suggested that articular C fibre afferents could make a significant neurogenic contribution to the initiation or maintenance of inflammatory joint disease.

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“…It is most probable that C fibres mediate neurogenic oedema (Chahl & Ladd, 1976b) and it would seem reasonable to suggest that any substance which produces pain should produce some component of neurogenic oedema. However it is not known whether the mechanism of release of the neurohumour from sensory nerve terminals is linked to the mechanisms involved in the production of action potentials in the nerve.…”

Section: Capsaicin Pretreatmentmentioning

confidence: 99%

Modification by Capsaicin and Compound 48/80 of Dye Leakage Induced by Irritants in the Rat

Arvier

Chahl

Ladd

1977

British J Pharmacology

Self Cite

104

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1Concentration-related dye leakage produced by intracutaneous injections of irritants was measured in rats by an Evans blue technique. 2 In rats pretreated with a total dose of 50 mg capsaicin over 4 days, the response to capsaicin, formalin, HC1, KCI, prostaglandin E,, bradykinin and bradykinin with prostaglandin E1 (10-6 M) were greatly reduced, the responses to histamine and 5-hydroxytryptamine were slightly reduced and those to adenosine 5'-triphosphate (ATP) and compound 48/80 were unaffected.3 Pretreatment with intracutaneous injections of compound 48/80 (0.5 ,ug, 24 and 48 h previously) recuded the responses to ATP, compound 48/80, HCI, KCI, prostaglandin E1, and bradykinin but did not affect those to histamine, 5-hydroxytryptamine or bradykinin with prostaglandin E1 (106 M). 4 Responses to capsaicin and formalin produced spotted blueing extending over a large area and were suppressed by compound 48/80 in the smaller pretreated area only. Capsaicin responses were reduced with larger doses of compound 48/80 (total dose 15 gg).

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Local oedema and general excitation of cutaneous sensory receptors produced by electrical stimulation of the saphenous nerve in the rat

Cited by 86 publications

References 11 publications

Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease.

Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn disease.

Extravasation in the knee induced by antidromic stimulation of articular C fibre afferents of the anaesthetized cat.

Modification by Capsaicin and Compound 48/80 of Dye Leakage Induced by Irritants in the Rat

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