Functional relationships between sensory nerve fibers and mast cells of dura mater in normal and inflammatory conditions

Dimitriadou, Violetta; Rouleau, A.; Tuong, M. Dam Trung; Newlands, GF; Miller, H. R. P.; Luffau, G.; Schwartz, Jean‐Charles; Garbarg, M.

doi:10.1016/s0306-4522(96)00488-5

Cited by 110 publications

(79 citation statements)

References 49 publications

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“…H 3 KO mice showed a complete loss of the H 3 RLI on this innervation, confirming the presence of neuronal H 3 Rs in the deep dermis of normal mice. The perivascular localization of these fibers is consistent with well known functional and anatomical associations between histamine-containing mast cells, blood vessels, and peptidergic afferent fibers (Imamura et al, 1996;Dimitriadou et al, 1997). H 3 RLI was found on A␤ fibers that terminate in Meissner's corpuscles in glabrous skin and as lanceolate endings in hairy skin, as well as on epidermal keratinocytes and Merkel cells (Cannon et al, 2007a), all of which coexpress CGRP immunoreactivity (Paré et al, 2001;Khodorova et al, 2003) (Fig.…”

Section: Histamine and H 3 Rs In The Nervous Systemsupporting

confidence: 83%

“…Inflammation provoked by many treatments (including antidromic nerve stimulation, formalin, capsaicin, zymosan, complete Freud's adjuvant, and bradykinin) is reduced by these drugs; end points measured include edema, plasma extravasation, and increases in vascular permeability. Local application of the agonists to heart (Imamura et al, 1996), lung (Delaunois et al, 1995), and dura mater (Dimitriadou et al, 1997) effectively reduced these inflammatory responses, strongly suggesting that H 3 Rs on local afferent fibers can attenuate peptide-mediated inflammation. The H 4 agonist properties of immepip and imetit (Lim et al, 2005) may or may not be relevant for inflammation research.…”

Section: Peripheral H 3 Rs and Inflammationmentioning

confidence: 92%

“…Inhibition of transmitter release at the spinal terminations of these deep dermal fibers has been proposed to account for this antinociceptive activity. Although the figure is based on immunohistochemical studies of the skin, DRG, and spinal cord, H 3 R activation is known to reduce inflammatory peptide release the heart (Imamura et al, 1996), lung (Delaunois et al, 1995), and dura mater (Dimitriadou et al, 1997 (Cannon et al, 2007b). Thus, studies in mice and rats with two different H 3 agonists Cannon et al, 2007b) suggest that inhibition of formalin flinching or licking is mediated by activation of spinal H 3 Rs on peptidergic afferent fibers.…”

Section: Formalin-induced Nociceptionmentioning

confidence: 99%

“…Such effects are thought to account for the well established anti-inflammatory properties of systemically and locally administered H 3 agonists. Active compounds include BP 2-94 , RAMH (Ohkubo et al, 1995;Dimitriadou et al, 1997;Poveda et al, 2006), imetit (Delaunois et al, 1995;Imamura et al, 1996), and immepip (Cannon et al, 2007b). Inflammation provoked by many treatments (including antidromic nerve stimulation, formalin, capsaicin, zymosan, complete Freud's adjuvant, and bradykinin) is reduced by these drugs; end points measured include edema, plasma extravasation, and increases in vascular permeability.…”

Section: Peripheral H 3 Rs and Inflammationmentioning

confidence: 99%

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H₃ Receptors and Pain Modulation: Peripheral, Spinal, and Brain Interactions

Hough¹,

Rice²

2010

J Pharmacol Exp Ther

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Histamine H 3 receptors (H 3 Rs), distributed within the brain, the spinal cord, and on specific types of primary sensory neurons, can modulate pain transmission by several mechanisms. In the skin, H 3 Rs are found on certain A␤ fibers, and on keratinocytes and Merkel cells, as well as on deep dermal, peptidergic A␦ fibers terminating on deep dermal blood vessels. Activation of H 3 Rs on the latter in the skin, heart, lung, and dura mater reduces calcitonin gene-related peptide and substance P release, leading to anti-inflammatory (but not antinociceptive) actions. However, activation of H 3 Rs on the spinal terminals of these sensory fibers reduces nociceptive responding to lowintensity mechanical stimuli and inflammatory stimuli such as formalin. These findings suggest that H 3 R agonists might be useful analgesics, but these drugs have not been tested in clinically relevant pain models. Paradoxically, H 3 antagonists/ inverse agonists have also been reported to attenuate several types of pain responses, including phase II responses to formalin. In the periaqueductal gray (an important pain regulatory center), the H 3 inverse agonist thioperamide releases neuronal histamine and mimics histamine's biphasic modulatory effects in thermal nociceptive tests. Newer H 3 inverse agonists with potent, selective, and brain-penetrating properties show efficacy in several neuropathic and arthritis pain models, but the sites and mechanisms for these actions remain poorly understood. Histamine and PainHistamine, found throughout the body in both neuronal and non-neuronal sources, can modify pain transmission by actions at multiple receptors in the skin, spinal cord, and brain. Rapidly expanding information on the distribution and functions of H 3 receptors (H 3 Rs) and the recent development of new H 3 R ligands have heightened interest in the possible modulation of pain by H 3 R-acting drugs. The present article provides a short, integrative overview of relevant studies (for review see also Sander et al., 2008;Tiligada et al., 2009;Gemkow et al., 2009). Measuring Pain in the LaboratoryPain, which can be defined as the central representation of tissue-damaging stimuli with sensory-discriminative, motivational, and cognitive components (Besson and Chaouch, 1987), is readily understood by humans as a sensory experience. Ideally, evaluation of the pain-relieving properties of drugs should directly measure reductions in pain perception. Instead, assessment of analgesic drug action in nonverbal subjects relies heavily on measures of behavioral, often reflexive, responses. Because drugs can modify these responses (but not necessarily the underlying perceptions), results from pain testing in laboratory animals can be misleading. The present limitations of preclinical methodologies for identifying pain-relieving drugs have been discussed previously Vierck et al., 2008).Notwithstanding the limitations in state-of-the-art analgesic testing, many factors must be considered when evaluating

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Section: Histamine and H 3 Rs In The Nervous Systemsupporting

confidence: 83%

Section: Peripheral H 3 Rs and Inflammationmentioning

confidence: 92%

Section: Formalin-induced Nociceptionmentioning

confidence: 99%

Section: Peripheral H 3 Rs and Inflammationmentioning

confidence: 99%

See 2 more Smart Citations

H₃ Receptors and Pain Modulation: Peripheral, Spinal, and Brain Interactions

Hough¹,

Rice²

2010

J Pharmacol Exp Ther

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“…Numerous studies have stressed the relevance of the morphological structure of dural innervation, in fact some interesting investigations in rats (12)(13)(14)(15)(16)(17) have focused on the peptidergic, catecholaminergic and nitroxidergic innervation of dura mater encephali (18), revealing a possible relationship with the etiopathogenesis of headache and dural pain (13,15,19,20).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical profile of neurotrophins in human cranial dura mater and meningiomas

et al. 2009

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Abstract. The immunohistochemical profile of neurotrophins and their receptors in the human cranial dura mater was studied by examining certain dural zones in specimens harvested from different regions (frontal, temporal, parietal and occipital). Dural specimens were obtained during neurosurgical operations performed in ten patients for surgical treatment of intracranial lesions (meningiomas, traumas, gliomas, vascular malformations). The dural fragments were taken from the area of the craniotomy at least 8 cm from the lesion as well as from the area in which the meningioma had its dural attachment. Immunohistochemical characterization and distribution of neurotrophins, with their receptors, were analyzed. The concrete role played by these neurotrophic factors in general regulation, vascular permeability, algic responsivity and release of locally active substances in the human dura mater is still controversial. Our study revealed a general structural alteration of dural tissue due to the invasivity of meningiomatous lesions, together with an improved expression of brain derived neurotrophic factor (BDNF) in highly proliferating neoplastic cells and an evident production of nerve growth factor (NGF) in inflammatory cells, suggesting that BDNF has a role in supporting the proliferation rate of neoplastic cells, while NGF is involved in the activation of a chronic inflammatory response in neoplastic areas. IntroductionMeningiomas are the most common benign intracranial tumors, but some meningiomas show malignancy with invasion into the surrounding structures, as well as a high recurrence rate and extracranial metastases (1). Meningiomas arise from arachnoidal cells, most of which lie in close proximity to the venous sinuses: in fact, this is the most common site for meningioma formation. They are most frequently attached to the dura mater over the superior parasagittal surface of the frontal and parietal lobes, along the sphenoid ridge, in the olfactory grooves, the Sylvian region, superior cerebellum along the falx cerebri, cerebellopontine angle and spinal cord. The tumor is usually well-circumscribed, with the base lying on the dura mater.Histologically, the cells are relatively uniform, with a tendency to form highly-circumscribed whorls and to generally disrupt the distribution and the structure of collagen fibers (main component of dural tissue) and to originate 'psammoma bodies' (laminated concretions) which can calcify and are often strongly vascularized.The remarkable proliferation rate and vascularisation which determine a rapid replacement of normal dural tissue by the neoplastic cells, is regulated by several different growth factors, such as NGF related to an increased activation of the inflammatory cells at the beginning of the neoplastic invasion and BDNF, involved in the increased activation of the tumoral cells.Neurotrophins (NTs), also known as neurotrophic factors, constitute a family of dimeric proteins working as polypeptidic growth factors and acting like extracellular ligands. NTs, including ...

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