NO-induced migraine attack: strong increase in plasma calcitonin gene-related peptide (CGRP) concentration and negative correlation with platelet serotonin release

Juhász, Gabriella; Zsombók, Terézia; Modos, Edit A.; Olajos, Sarolta; Jakab, Balázs; Németh, József; Szolcsányi, Janós; Vitrai, József; Bagdy, György

doi:10.1016/j.pain.2003.09.008

Cited by 242 publications

(239 citation statements)

References 49 publications

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“…CGRP is believed to play an important role in the genesis and maintenance of inflammation and pain associated with both migraine and TMJ pathology (Lassen et al, 2002;Juhasz et al, 2003;Lobbezoo et al, 2004). In this study, we used an in vivo model of TMJ inflammation to investigate the effect of Theobroma cacao extract on trigeminal nerve activation and CGRP release.…”

Section: Discussionmentioning

confidence: 99%

Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract

Abbey

Patil

Vause

et al. 2008

Journal of Ethnopharmacology

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Ethnopharmacological relevance-Cocoa bean preparations were first used by the ancient Maya and Aztec civilizations of South America to treat a variety of medical ailments involving the cardiovascular, gastrointestinal, and nervous systems. Diets rich in foods containing abundant polyphenols, as found in cocoa, underlie the protective effects reported in chronic inflammatory diseases. Release of calcitonin gene-related peptide (CGRP) from trigeminal nerves promotes inflammation in peripheral tissues and nociception.Aim of the study-To determine whether a methanol extract of Theobroma cacao L. (Sterculiaceae) beans enriched for polyphenols could inhibit CGRP expression, both an in vitro and an in vivo approach was taken.Results-Treatment of rat trigeminal ganglia cultures with depolarizing stimuli caused a significant increase in CGRP release that was repressed by pretreatment with Theobroma cacao extract. Pretreatment with Theobroma cacao was also shown to block the KCl-and capsaicin-stimulated increases in intracellular calcium. Next, the effects of Theobroma cacao on CGRP levels were determined using an in vivo model of temporomandibular joint (TMJ) inflammation. Capsaicin injection into the TMJ capsule caused an ipsilateral decrease in CGRP levels. Theobroma cacao extract injected into the TMJ capsule 24 h prior to capsaicin treatment repressed the stimulatory effects of capsaicin.Conclusions-Our results demonstrate that Theobroma cacao extract can repress stimulated CGRP release by a mechanism that likely involves blockage of calcium channel activity. Furthermore, our findings suggest that the beneficial effects of diets rich in cocoa may include suppression of sensory trigeminal nerve activation.

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Section: Discussionmentioning

confidence: 99%

Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract

Abbey

Patil

Vause

et al. 2008

Journal of Ethnopharmacology

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“…60 Further experiments have provided supportive data demonstrating a linear correlation between the increased levels of CGRP and the intensity of the headache. 61,62 It is worth noting that low pain results in no significant increase in venous CGRP. 62,63 In addition, nitroglycerine did not elicit cluster headache attacks if the patient was not in a prone status (i.e., a state in which the disease was active and a small stimulation could then elicit the full cluster headache attack).…”

Section: Neurotransmitter Release In Migrainementioning

confidence: 99%

CGRP Receptor Antagonism and Migraine

Edvinsson

2010

Neurotherapeutics

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Summary: Calcitonin gene-related peptide (CGRP) is expressed throughout the central and peripheral nervous systems, consistent with control of vasodilatation, nociception, motor function, secretion, and olfaction. ␣CGRP is prominently localized in primary spinal afferent C and A⌬ fibers of sensory ganglia, and ␤CGRP is the main isoform in the enteric nervous system. In the CNS there is a wide distribution of CGRP-containing neurons, with the highest levels occurring in striatum, amygdala, colliculi, and cerebellum. The peripheral projections are involved in neurogenic vasodilatation and inflammation, and central release induces hyperalgesia. CGRP is released from trigeminal nerves in migraine. Trigeminal nerve activation results in antidromic release of CGRP to cause non-endothelium-mediated vasodilatation. At the central synapses in the trigeminal nucleus caudalis, CGRP acts postjunctionally on second-order neurons to transmit pain signals centrally via the brainstem and midbrain to the thalamus and higher cortical pain regions. Recently developed CGRP receptor antagonists are effective at aborting acute migraine attacks. They may act both centrally and peripherally to attenuate signaling within the trigeminovascular pathway.

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“…There is evidence that intravenous infusion of CGRP produces a migraine-like headache [66], and intravenous infusion of nitric oxide produces a migraine-like headache with an associated increase in plasma CGRP levels [67]. In migraine patients baseline CGRP levels were considerably higher, and the changes in plasma CGRP levels during migraine attacks were significantly correlated with the headache intensity [67].…”

Section: Migraine and Neurogenic Inflammationmentioning

confidence: 99%

CGRP and migraine: neurogenic inflammation revisited

Geppetti

Capone²,

Trevisani

et al. 2005

J Headache Pain

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The term 'neurogenic inflammation' refers to a series of proinflammatory responses produced by the stimulation of peripheral terminals of a subset of primary sensory neurons and the subsequent release of the neuropeptides, calcitonin gene-related peptide (CGRP) and the tachykinins, substance P (SP) and neurokinin A (NKA) [1]. The neurons that produce inflammation comprise a heterogeneous cell population with A-delta and C fibres, defined as polymodal nociceptors because they sense thermal, chemical and high-threshold mechanical stimuli. These neurons express on their plasma membrane a large panel of excitatory and inhibitory receptors and channels, and some of these signalling proteins have been successfully used as targets for analgesic or anti-inflammatory drugs. Among the channels expressed on peptidergic primary sensory neurons, transient receptor potential vanilloid-1 (TRPV1) [2], activated by the xenobiotic capsaicin, the pungent ingredient of plants of the genus Capsicum, is of paramount importance. Capsaicin produces burning pain by stimulating TRPV1 and by releasing sensory neuropeptides causes neurogenic inflammation. However, high concentrations/doses of capsaicin have the ability, after an initial excitatory phase, to desensitise the sensory nerve terminals, thus reducing the transmission of sensory/pain signals and abolishing neurogenic inflammation [3, 4]. This specific feature of capsaicin has greatly contributed to define the role of this subset of sensory nerves in pathophysiological models of human diseases and has been Pierangelo Geppetti Jay Guido Capone Marcello Trevisani Paola Nicoletti Giovanni Zagli Maria Rosalia Tola Abstract For more than a century neurogenic inflammation has been proposed to have a role in various human diseases. The present review will cover the conceptual steps of the itinerary that has led to the conclusion that neurogenic inflammation is important in migraine. Of particular relevance for the object of this article is the observation that tachykinindependent neurogenic inflammatory responses are evident in rodents, but much less pronounced or absent in other mammal species, including man, whereas neurogenic vasodilatation, most likely mediated by CGRP, occurs in most mammalian species and also in man. Recent evidence that a CGRP receptor antagonist was effective in the treatment of migraine attack supports the hypothesis that neurogenic vasodilatation is a major underlying mechanism of migraine.

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NO-induced migraine attack: strong increase in plasma calcitonin gene-related peptide (CGRP) concentration and negative correlation with platelet serotonin release

Cited by 242 publications

References 49 publications

Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract

Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract

CGRP Receptor Antagonism and Migraine

CGRP and migraine: neurogenic inflammation revisited

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