On Pain Mechanisms in Cluster Headache

Hardebo, Jan Erik

doi:10.1111/j.1526-4610.1991.hed3102091.x

Cited by 47 publications

(20 citation statements)

References 47 publications

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“…vasodilatation and plasma extravasation in the dura mater, have been proposed as an essential mechanism for migraine pain and other headaches (Moskowitz, 1984;Hardebo, 1990). In the rat a neurogenic inflammation of the dura mater was provoked by stimulation of trigeminal afferents, indicated by symptoms like plasma extravasation (Markowitz et al, 1987), aggregation and adhesion of platelets, and activation of mast cells (Dimitriadou et al, 1991;1992).…”

Section: Introductionmentioning

confidence: 99%

Increase of meningeal blood flow after electrical stimulation of rat dura mater encephali: mediation by calcitonin gene‐related peptide

Kurosawa

Meßlinger

Pawlak

et al. 1995

British J Pharmacology

137

117

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Japan1 The dura mater encephali of the rat was exposed and the blood flow around branches of the medial meningeal artery was monitored with a laser Doppler flowmeter. Changes in the meningeal blood flow (MBF) following electrical stimulation of the dura mater at a parasagittal site were registered. The effects of human calcitonin gene-related peptide (h-aCGRP) and the CGRP antagonist (h-aCGRP8-37) on the MBF were tested. 2 Electrical stimulation with rectangular pulses of 0.5 ms, 10-20 V, 5-10 Hz and a duration of 30 s caused an increase of the MBF in 14 out of 16 rats tested. The increases were dependent on stimulus strength and frequency. 3 The increase in MBF was inhibited in a dose-dependent manner by topical application of 0.1 ml of h-mCGRP837 at concentrations of 10-7-10-'M. The highest dose abolished the increase in MBF. 4 Topical administration of 0.1 ml of h-aCGRP at a concentration of 10-4 M increased the basal MBF by 15% on average. 5 It is suggested that the increase in MBF following electrical stimulation of the dura mater is mediated by the release of CGRP. The contribution of the dural afferent and sympathetic and parasympathetic efferent nerve fibres to this response are discussed.

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Section: Introductionmentioning

confidence: 99%

Increase of meningeal blood flow after electrical stimulation of rat dura mater encephali: mediation by calcitonin gene‐related peptide

Kurosawa

Meßlinger

Pawlak

et al. 1995

British J Pharmacology

137

117

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“…CGRP is found in a proportion of intracranial sensory nerves which arise from the trigeminal ganglia [24, 25, 26]. Increased levels of CGRP have been measured during spontaneous and experimentally induced attacks of migraine and cluster headache [27, 28, 29, 30, 31]. In animal experiments, CGRP is released from meningeal structures by electrical stimulation of the trigeminal ganglion and the dura mater in vivo and in vitro [32, 33].…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Releases Calcitonin-Gene-Related Peptide from Rat Dura mater Encephali Promoting Increases in Meningeal Blood Flow

2002

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Nitric oxide (NO) and calcitonin-gene-related peptide (CGRP) are implicated in the pathophysiology of vascular headaches. We studied the interaction of these two vasodilatory mediators in an animal model and suggest that NO may increase meningeal blood flow not only by its direct vasodilatory action but also by stimulating CGRP release. First, CGRP release from the rat cranial dura mater was measured in vitro using an enzyme immunoassay. Hemisected skulls with adhering dura mater were filled with synthetic interstitial fluid and stimulated with the NO donor diethylamine-NONOate (10^–5–10^–3M) or with NO gas (1,000 ppm), which caused concentration-dependent increases in CGRP release up to 166.8%. Second, meningeal blood flow was recorded in vivo in the exposed dura mater using laser Doppler flowmetry. Topical application of the NO donors NONOate, S-nitroso-N-acetylpenicillamine and N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino)-ethenamine (10^–5–10^–3M) caused concentration-dependent increases in blood flow. These increases were significantly reduced by local preliminary application of the CGRP receptor antagonist CGRP_8–37 (10^–4M). We conclude that NO stimulates the release of CGRP from dural afferents. The blood-flow-increasing effect of NO seems to be partly mediated by CGRP. The interaction of NO and CGRP may be relevant for the development of vascular headaches.

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“…SPG neurons receive projections from the superior salivatory nucleus and both sympathetic and sensory neurons course through the ganglion as well [7]. SPG neurons innervate the cerebral vasculature, nasal, palatine and lacrimal glands, and thus, regulate cerebral blood flow and secretion from the aforementioned glands [8]. Few electrophysiological studies have been undertaken to examine signaling mechanisms that couple Ca 2+ channels and G protein-coupled…”

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confidence: 99%

Electrophysiological and immunofluorescence characterization of Ca2+ channels of acutely isolated rat sphenopalatine ganglion neurons

Margas

Ruiz‐Velasco

2007

Neuroscience Letters

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SummaryThe sphenopalatine ganglion (SPG) is the main parasympathetic ganglion that is involved in regulating cerebral vascular tone and gland secretion. SPG neurons have been implicated in some types of migraine headaches but their precise role has yet to be determined. In addition, very little information is available regarding ion channel modulation by neurotransmitters that are involved in the parasympathetic drive of SPG neurons. In this study, acute isolation of adult rat SPG neurons was developed in order to begin the electrophysiological characterization of this ganglion. Under our dissociation conditions, the average number of neurons obtained per ganglion was greater than 1200.Immunofluorescence imaging results showed positive labeling with acethylcholinesterase (AChE), confirming the parasympathetic nature of SPG neurons. On the other hand, weak tyrosine hydroxylase immunostaining was observed in these neurons. Whole-cell patch-clamp recordings revealed that most of the Ca 2+ current is carried by N-type (53%) and SNX-482 resistant R-type (30%) Ca 2+ channels. In addition, Ca 2+ currents were inhibited in a voltage-dependent manner following exposure to oxotremorine-M (Oxo-M), norepinephrine and ATP via muscarinic acetylcholine receptor 2 (M 2 AChR) subtype, adrenergic and P2Y purinergic receptors, respectively. The peptides VIP and angiotensin II failed to modulate Ca 2+ currents, suggesting that these receptors are not present on the SPG soma or do not couple to Ca 2+ channels. In summary, our data suggest that the Ca 2+ current inhibition mediated by Oxo-M, NE and ATP in adult rat SPG neurons plays an integral part in maintaining parasympathetic control of cranial functions. Keywords sphenopalatine ganglion; parasympathetic; N-type Ca 2+ channels; whole-cell patch-clamp; immunofluorescenceThe sphenopalatine ganglion (SPG) is part of the parasympathetic branch of the autonomic nervous system and is located in the pterygopalatine fossa beneath the maxillary nerve [7]. SPG neurons receive projections from the superior salivatory nucleus and both sympathetic and sensory neurons course through the ganglion as well [7]. SPG neurons innervate the cerebral vasculature, nasal, palatine and lacrimal glands, and thus, regulate cerebral blood flow and secretion from the aforementioned glands [8]. Few electrophysiological studies have been undertaken to examine signaling mechanisms that couple Ca 2+ channels and G protein-coupledCorresponding author: Victor Ruiz-Velasco, Department of Anesthesiology, H187, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033-0850, Phone: 717-531-6076, FAX: 717-531-6221, e-mail: vruizvelasco@psu.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the producti...

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On Pain Mechanisms in Cluster Headache

Cited by 47 publications

References 47 publications

Increase of meningeal blood flow after electrical stimulation of rat dura mater encephali: mediation by calcitonin gene‐related peptide

Increase of meningeal blood flow after electrical stimulation of rat dura mater encephali: mediation by calcitonin gene‐related peptide

Nitric Oxide Releases Calcitonin-Gene-Related Peptide from Rat Dura mater Encephali Promoting Increases in Meningeal Blood Flow

Electrophysiological and immunofluorescence characterization of Ca2+ channels of acutely isolated rat sphenopalatine ganglion neurons

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