Catecholaminergic and acetylcholine esterase containing nerves of cranial and spinal dura mater in humans and rodents

Artico, Marco; Cavallotti, Carlo

doi:10.1002/jemt.1085

Cited by 45 publications

(35 citation statements)

References 60 publications

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“…Mast cells are distributed in spinal dura-arachnoid, 19,20,40 and often aligned with local arachnoid vessels. 41 The meningeal mast cells are subject to degranulation by the local milieu.…”

Section: Discussionmentioning

confidence: 99%

Role of Meningeal Mast Cells in Intrathecal Morphine–evoked Granuloma Formation

Yaksh¹,

Allen

Veesart³

et al. 2013

Anesthesiology

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Background Intrathecal morphine forms granulomas that arise from the adjacent arachnoid membrane. We propose that these inflammatory cells exit the meningeal vasculature secondary to meningeal mast cell degranulation. Methods Three sets of experiments were accomplished in dogs. 1) Ex vivo Meningeal mast cell degranulation. Histamine release was measured ex vivo from canine dura incubated with opiates. 2) In vivo cutaneous mast cell degranulation. Flare areas on the dog abdomen were measured after subcutaneous opiates. 3) In vivo granuloma pharmacology. Dogs with lumbar intrathecal catheters received infusion of intrathecal saline or intrathecal morphine. Intrathecal morphine dogs received: i) No other treatment (Control); ii) Twice daily subcutaneous naltrexone; iii) Intrathecal co-infusion of cromolyn; or, iv) Twice daily subcutaneous cromolyn for the 24–28 day study course. Results 1) Morphine but not fentanyl evoked dural histamine release, which was blocked by cromolyn but not naloxone. 2) Wheal/flare was produced by subcutaneous morphine, methadone, hydromorphone, but not fentanyl, and was unaffected by naltrexone but prevented by cromolyn. 3) Granulomas occurred in all dogs receiving intrathecal morphine (15/15); subcutaneous naltrexone had no effect on granulomas (6/6), but was reduced by concurrent intrathecal cromolyn (0/5) or twice daily subcutaneous cromolyn (1 of 5). Conclusions The pharmacology of cutaneous/dural MC degranulation and intrathecal granulomas are comparable, not mediated by opioid receptors, and reduced by agents preventing MC degranulation. If an agent produces cutaneous MC degranulation at concentrations produced by intrathecal delivery, the agent may initiate granulomas.

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“…Mast cells are distributed in spinal dura-arachnoid, 19,20,40 and often aligned with local arachnoid vessels. 41 The meningeal mast cells are subject to degranulation by the local milieu.…”

Section: Discussionmentioning

confidence: 99%

Role of Meningeal Mast Cells in Intrathecal Morphine–evoked Granuloma Formation

Yaksh¹,

Allen

Veesart³

et al. 2013

Anesthesiology

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“…However, the meninges surrounding the brain are also innervated by trigeminal nociceptive fibers in close proximity to dense populations of resident immune cells. Indeed the meningeal immune population includes fibroblasts, macrophages, dendritic cells, and mast cells (Artico and Cavallotti, 2001; Braun et al, 1993; Fischer and Reichmann, 2001; McMenamin, 1999; Mercier and Hatton, 2004; Rozniecki et al, 1999; Zenker et al, 1994), each of which are capable of releasing proinflammatory, neuroexcitatory mediators.…”

Section: Introductionmentioning

confidence: 99%

A novel method for modeling facial allodynia associated with migraine in awake and freely moving rats

Wieseler

Ellis

Sprunger

et al. 2010

Journal of Neuroscience Methods

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Migraine is a neurovascular disorder that induces debilitating headaches associated with multiple symptoms including facial allodynia, characterized by heightened responsivity to normally innocuous mechanical stimuli. It is now well accepted that immune activation and immune-derived inflammatory mediators enhance pain responsivity, including in the trigeminal system. Nociceptive ("pain" responsive) trigeminal nerves densely innervate the cranial meninges. We have recently proposed that the meninges may serve as a previously unidentified, key interface between the peripheral immune system and the CNS with potential implications for understanding underlying migraine mechanisms. Our focus here is the development of a model for facial allodynia associated with migraine. We developed a model wherein an indwelling catheter is placed between the skull and dura, allowing immunogenic stimuli to be administered over the dura in awake and freely moving rats. Since the catheter does not contact the brain itself, any proinflammatory cytokines induced following manipulation derive from resident or recruited meningeal immune cells. While surgery alone does not alter immune activation markers, TNF or IL6 mRNA and/or protein, it does decrease gene expression and increase protein expression of IL-1 at 4 days after surgery. Using this model we show the induction of facial allodynia in response to supradural administration of either the HIV glycoprotein gp120 or inflammatory soup (bradykinin, histamine, serotonin, and prostaglandin E2), and the induction of hindpaw allodynia in our model after inflammatory soup. This model allows time and dose dependent assessment of the relationship between changes in meningeal inflammation and corresponding exaggerated pain behaviors.

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“…Although the dura mater is the intracranial structure most heavily innervated by pain fibers, it is also populated by resident mast cells (MCs) in both humans (Artico and Cavallotti, 2001) and rodents (Dimlich et al, 1991;Rozniecki et al, 1999;. These granulated immunocompetent cells, which reside near blood vessels and in apposition to the meningeal nociceptive fibers (Rozniecki et al, 1999), have the capacity to initiate or amplify inflammatory responses by releasing a host of mediators such as histamine, serotonin, cytokines, and various lipid mediators, including leukotrienes (LTs) and prostaglandins (PGs) (Metcalfe et al, 1997;Mekori and Metcalfe, 2000).…”

mentioning

confidence: 99%

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Zhang¹,

Strassman²,

Burstein³

et al. 2007

J Pharmacol Exp Ther

150

125

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Intracranial headaches such as migraine are thought to result from activation of sensory trigeminal pain neurons that supply intracranial blood vessels and the meninges, also known as meningeal nociceptors. Although the mechanism underlying the triggering of such activation is not completely understood, our previous work indicates that the local activation of the inflammatory dural mast cells can provoke a persistent sensitization of meningeal nociceptors. Given the potential importance of mast cells to the pain of migraine it is important to understand which mast cell-derived mediators interact with meningeal nociceptors to promote their activation and sensitization. In the present study, we have used in vivo electrophysiological single-unit recording of meningeal nociceptors in the trigeminal ganglion of anesthetized rats to examine the effect of a number of mast cell mediators on the activity level and mechanosensitivity of meningeal nociceptors. We have found that that serotonin (5-HT), prostaglandin I 2 (PGI 2 ), and to a lesser extent histamine can promote a robust sensitization and activation of meningeal nociceptors, whereas the inflammatory eicosanoids PGD 2 and leukotriene C 4 are largely ineffective. We propose that dural mast cells could promote headache by releasing 5-HT, PGI 2 , and histamine.

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Catecholaminergic and acetylcholine esterase containing nerves of cranial and spinal dura mater in humans and rodents

Cited by 45 publications

References 60 publications

Role of Meningeal Mast Cells in Intrathecal Morphine–evoked Granuloma Formation

Role of Meningeal Mast Cells in Intrathecal Morphine–evoked Granuloma Formation

A novel method for modeling facial allodynia associated with migraine in awake and freely moving rats

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

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