Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Ottosson, Anders; Edvinsson, Lars

doi:10.1046/j.1468-2982.1997.1703166.x

Cited by 187 publications

(138 citation statements)

References 51 publications

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“…PGP 9.5 reactivity identifies all cutaneous nerves, 51,56 whereas only a fraction of such nerves produce CGRP. 52,56 Notably, the neuropeptide CGRP can induce degranulation of certain mast cell populations, 16,19,20 including dermal mast cells in both humans 16 and mice. 19 Accordingly, CHS in response to OX represents a setting in which mast cells contribute to the elongation of nerves that can, in turn, produce a neuropeptide with the capacity to induce functional responses in dermal mast cells.…”

Section: Discussionmentioning

confidence: 99%

Mast Cell-Derived Tumor Necrosis Factor Can Promote Nerve Fiber Elongation in the Skin during Contact Hypersensitivity in Mice

Kakurai

Monteforte

Suto

et al. 2006

The American Journal of Pathology

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In humans, lesions of contact eczema or atopic dermatitis can exhibit increases in epidermal nerves, but the mechanism resulting in such nerve elongation are not fully understood. We found that contact hypersensitivity reactions to oxazolone in mice were associated with significant increases in the length of nerves in the epidermis and dermis. Using genetically mast cell-deficient c-kit mutant mice selectively repaired of their dermal mast cell deficiency with either wild-type or tumor necrosis factor (TNF)-deficient mast cells, we found that mast cells, and mast cell-derived TNF, significantly contributed to the elongation of epidermal and dermal PGP 9.5 ؉ nerves and dermal CGRP ؉ nerves, as well as to the inflammation observed at sites of contact hypersensitivity in response to oxazolone. Moreover, the percentage of mast cells in close proximity to dermal PGP 9.5 ؉ nerve fibers was significantly higher in wild-type mice and in c-kit mutant mice repaired of their dermal mast cell deficiency by the adoptive transfer of wild-type mast cells than in TNF-deficient mice or in TNF ؊/؊ mast cell-engrafted c-kit mutant mice. These observations show that mast cells, and mast cell-derived TNF, can promote the elongation of cutaneous nerve fibers during contact hypersensitivity in the mouse.

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Section: Discussionmentioning

confidence: 99%

Mast Cell-Derived Tumor Necrosis Factor Can Promote Nerve Fiber Elongation in the Skin during Contact Hypersensitivity in Mice

Kakurai

Monteforte

Suto

et al. 2006

The American Journal of Pathology

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“…44 Furthermore, VIP releases a relatively small proportion (10%) of histamine from human dural mast cells, compared with CGRP (10% vs 32%). 45 Thus, it seems unlikely (although it remains to be investigated) that PACAP can induce sufficient mast cell degranulation in the perivascular space of cranial arteries to result in nociceptive input.…”

Section: The Peripheral Actions Of Pacapmentioning

confidence: 99%

The PACAP Receptor: A Novel Target for Migraine Treatment

2010

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Summary:The origin of migraine pain has not yet been clarified, but accumulating data point to neuropeptides present in the perivascular space of cranial vessels as important mediators of nociceptive input during migraine attacks. Pituitary adenylate cyclase-activating polypeptide (PACAP) is present in sensory trigeminal neurons and may modulate nociception at different levels of the nervous system. Human experimental studies have shown that PACAP-38 infusion induces marked dilatation of extracerebral vessels and delayed migraine-like attacks in migraine patients. PACAP selectively activates the PAC 1 receptor, which suggests a possible signaling pathway implicated in migraine pain. This review summarizes the current evidence supporting the involvement of PACAP in migraine pathophysiology and the PAC 1 receptor as a possible novel target for migraine treatment.

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“…CGRP is also implicated in modulating synaptic transmission of glutamate and acetylcholine [50][51][52]. In the periphery, release of CGRP from trigeminal fibers is believed to cause vasodilation and mast cell degranulation, ultimately resulting in a persistent pro-inflammatory sensitization of trigeminal nociceptors [53][54][55]. Studies have suggested that CGRP release works in a paracrine manner, causing excitation of nearby neuronal and satellite glial cells and stimulating its own synthesis [56].…”

Section: Functionmentioning

confidence: 99%

Targeting CGRP: A New Era for Migraine Treatment

Goldberg

Silberstein

2015

CNS Drugs

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Migraine is a highly prevalent headache disease that typically affects patients during their most productive years. Despite significant progress in understanding the underlying pathophysiology of this disorder, its treatment so far continues to depend on drugs that, in their majority, were not specifically designed for this purpose. The neuropeptide calcitonin gene-related peptide (CGRP) has been indicated as playing a critical role in the central and peripheral pathways leading to a migraine attack. It is not surprising that drugs designed to specifically block its action are gaining remarkable attention from researchers in the field with, at least so far, a safe risk profile. In this article, we highlight the evolution from older traditional treatments to the innovative CGRP target drugs that are revolutionizing the way to approach this debilitating neurological disease. We provide a brief introduction on pathophysiology of migraine and details on the characteristic, function, and localization of CGRP to then focus on CGRP receptor antagonists (CGRP-RAs) and CGRP monoclonal antibodies (CGRP mAbs). Key PointsThe neuropeptide calcitonin gene-related peptide (CGRP) has been indicated as playing a critical role in the central and peripheral pathways leading to a migraine attack.Targeting CGRP as a specific therapeutic tool for migraine may offer similar or even better efficacy than currently available treatments without the vasoconstrictive risk factors.Further studies are necessary to determine the exact role of CGRP receptor antagonists and CGRP monoclonal antibodies in migraine with aura, allodynia, and photophobia.

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Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Cited by 187 publications

References 51 publications

Mast Cell-Derived Tumor Necrosis Factor Can Promote Nerve Fiber Elongation in the Skin during Contact Hypersensitivity in Mice

Mast Cell-Derived Tumor Necrosis Factor Can Promote Nerve Fiber Elongation in the Skin during Contact Hypersensitivity in Mice

The PACAP Receptor: A Novel Target for Migraine Treatment

Targeting CGRP: A New Era for Migraine Treatment

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