Histamine and Migraine

Yuan, Hsiangkuo; Silberstein, Stephen D.

doi:10.1111/head.13164

Cited by 53 publications

(35 citation statements)

References 86 publications

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“…Present data show that, by targeting the H 1 receptor subtype, histamine evokes PMA in mice and provides indirect support to the contribution of the H 1 receptor, rather than H 2 receptors [51], in provoking migraine [52], and to the desensitization process that is supposed to ameliorate migraine [53]. It should be underlined that, despite the ability of histamine to sensitise nociceptors via H 1 receptor activation, the H 1 -antagonists were not always effective in reducing migraine [54].…”

Section: Discussionmentioning

confidence: 99%

Migraine-provoking substances evoke periorbital allodynia in mice

et al. 2019

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BackgroundAdministration of endogenous mediators or exogenous chemicals in migraine patients provoke early headaches and delayed migraine-like attacks. Although migraine provoking substances are normally vasodilators, dilation of arterial vessels does not seem to be the sole contributing factor, and the underlying mechanisms of the delayed migraine pain are mostly unknown. Sustained mechanical allodynia is a common response associated with the local administration of various proalgesic substances in experimental animals and humans. Here, we investigated the ability of a series of endogenous mediators which provoke or do not provoke migraine in patients, to cause or not cause mechanical allodynia upon their injection in the mouse periorbital area.MethodsMechanical allodynia was assessed with the von Frey filament assay. Stimuli were given by subcutaneous injection in the periorbital area of C57BL/6J mice; antagonists were administered by local and systemic injections.ResultsCalcitonin gene related peptide (CGRP), but not adrenomedullin and amylin, pituitary adenylyl cyclase activating peptide (PACAP), but not vasoactive intestinal polypeptide (VIP), histamine, prostaglandin E2 (PGE2) and prostacyclin (PGI2), but not PGF2α, evoked a dose-dependent periorbital mechanical allodynia. The painful responses were attenuated by systemic or local (periorbital) administration of antagonists for CGRP (CLR/RAMP1), PACAP (PAC-1), histamine H1, PGE2 (EP4), and PGI2 (IP) receptors, respectively.ConclusionsThe correspondence between substances that provoke (CGRP; PACAP, histamine, PGE2, PGI2), or do not provoke (VIP and PGF2α), migraine-like attacks in patients and periorbital allodynia in mice suggests that the study of allodynia in mice may provide information on the proalgesic mechanisms of migraine-provoking agents in humans. Results underline the ability of migraine-provoking substances to initiate mechanical allodynia by acting on peripheral terminals of trigeminal afferents.

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Section: Discussionmentioning

confidence: 99%

Migraine-provoking substances evoke periorbital allodynia in mice

et al. 2019

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“…If CGRP is not involved, it is reasonable to suggest that the release of other molecules from autonomic fibers mediate the arterial dilatation and the PPE by CSD. These may include aden-osine (Honey et al, 2002), histamine (Lassen et al, 2003;Yuan and Silberstein, 2018), pituitary adenylate cyclase-activating polypeptide (Seki et al, 1995;Schytz et al, 2009;Amin et al, 2012;Syed et al, 2012), nitric oxide (Moncada et al, 1988;Iversen et al, 1989;Buchanan and Phillis, 1993) and a respective localized activation/inhibition of parasympathetic/sympathetic fibers innervating the dura (Brennan et al, 2007;Busija et al, 2008). The cerebral venous system consists of large dural sinuses and cerebral veins (Schaller, 2004;Kiliç and Akakin, 2008).…”

Section: Discussionmentioning

confidence: 99%

CSD-Induced Arterial Dilatation and Plasma Protein Extravasation Are Unaffected by Fremanezumab: Implications for CGRP's Role in Migraine with Aura

et al. 2019

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Cortical spreading depression (CSD) is a wave of neuronal depolarization thought to underlie migraine aura. Calcitonin gene-related peptide (CGRP) is a potent vasodilator involved in migraine pathophysiology. Evidence for functional connectivity between CSD and CGRP has triggered scientific interest in the possibility that CGRP antagonism may disrupt vascular responses to CSD and the ensuing plasma protein extravasation (PPE). Using imaging tools that allow us to generate continuous, live, high-resolution views of spatial and temporal changes that affect arteries and veins in the dura and pia, we determined the extent to which CGRP contributes to the induction of arterial dilatation or PPE by CSD in female rats, and how these events are affected by the anti-CGRP monoclonal antibody (anti-CGRP-mAb) fremanezumab. We found that the CSD-induced brief dilatation and prolonged constriction of pial arteries, prolonged dilatation of dural arteries and PPE are all unaffected by fremanezumab, whereas the brief constriction and prolonged dilatation of pial veins are affected. In comparison, although CGRP infusion gave rise to the expected dilatation of dural arteries, which was effectively blocked by fremanezumab, it did not induce dilatation in pial arteries, pial veins, or dural veins. It also failed to induce PPE. Regardless of whether the nociceptors become active before or after the induction of arterial dilatation or PPE by CSD, the inability of fremanezumab to prevent them suggests that these events are not mediated by CGRP, a conclusion with important implications for our understanding of the mechanism of action of anti-CGRP-mAbs in migraine prevention.The current study identifies fundamental differences between two commonly used models of migraine, CSD induction and systemic CGRP infusion. It raises the possibility that conclusions drawn from one model may not be true or relevant to the other. It sharpens the need to accept the view that there is more than one truth to migraine pathophysiology and that it is unlikely that one theory will explain all types of migraine headache or the mechanisms of action of drugs that prevent it. Regarding the latter, it is concluded that not all vascular responses in the meninges are born alike and, consequently, that drugs that prevent vascular dilatation through different molecular pathways may have different therapeutic outcomes in different types of migraine.

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“…and pathological (allergic diseases, migraine, neuropsychiatric disorders, etc.) processes [98,99,100,101,102,103]. In cancer, histamine plays a critical role in cell proliferation, migration, and invasion, increasing the resistance to anticancer drug and the expression of markers (i.e., aldehyde dehydrogenase 1) in cancer-initiating cells [104].…”

Section: Gpcrs Activated By Inflammation-related Molecules In Ovarmentioning

confidence: 99%

G Protein-Coupled Receptors (GPCRs)-Mediated Calcium Signaling in Ovarian Cancer: Focus on GPCRs activated by Neurotransmitters and Inflammation-Associated Molecules

Predescu

Creţoiu

Crețoiu

et al. 2019

IJMS

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G-coupled protein receptors (GCPR) involve several signaling pathways, some of them being coupled with intracellular calcium (Ca2+) mobilization. GPCRs were involved in migration, invasion and metastasis of different types of cancers, including ovarian cancer. Many studies have discussed the essential contribution of GPCRs activated by steroid hormones in ovarian cancer. However, ovarian cancer is also associated with altered signals coming from the nervous system, the immune system or the inflammatory environment, in which GPCRs are ‘sensing’ these molecular signals. Many studies have been oriented so far on ovarian cell lines (most of them being of human cell lines), and only few studies based on animal models or clinical studies have been devoted to the expression changes or functional role of GPCRs in ovarian cancer. In this paper, we review the alterations of GPCRs activated by neurotransmitters (muscarinic receptors, serotonin receptors, dopamine receptors, adrenoceptors) or inflammation-associated molecules (bradykinin receptors, histamine receptors, chemokine receptors) in ovarian cancer and we discuss their potential as histological biomarkers.

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Histamine and Migraine

Cited by 53 publications

References 86 publications

Migraine-provoking substances evoke periorbital allodynia in mice

Migraine-provoking substances evoke periorbital allodynia in mice

CSD-Induced Arterial Dilatation and Plasma Protein Extravasation Are Unaffected by Fremanezumab: Implications for CGRP's Role in Migraine with Aura

G Protein-Coupled Receptors (GPCRs)-Mediated Calcium Signaling in Ovarian Cancer: Focus on GPCRs activated by Neurotransmitters and Inflammation-Associated Molecules

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