Migraine

Moskowitz, Michael A.; Buzzi, Maria Gabriella

doi:10.1016/s0072-9752(10)97021-8

Cited by 11 publications

(7 citation statements)

References 102 publications

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“…Clinical and experimental studies have proposed that a neuroinflammatory state of meninges, enriched with inflammatory cells releasing pain mediators like TNFα [50], known to play an important role in chronic pain [51], might contribute to migraine attacks [30], [31]. We recently provided first evidence for a proinflammatory profile, both in vivo and in vitro , in R192Q KI trigeminal ganglia, which suggests that neuroinflammation may occur also in this migraine mouse model [26].…”

Section: Discussionmentioning

confidence: 81%

“…As recently reviewed [28], [29], the cellular effects of TNFα are mediated by two distinct receptor classes (TNFR1 and TNFR2).While TNFR1 is ubiquitously expressed and is canonically considered to be a pro-apoptotic signal in cell death pathways, TNFR2 expression is restricted to immune cells like microglia and macrophages, neurons and oligodendrocytes. In view of previous reports that neuroinflammation might be contributory to sensitize neurons in migraine attacks [9], [18], [30], [31], we first investigated whether mouse trigeminal ganglion neurons could respond to TNFα as evidenced by their expression of the TNFα receptor TNFR2 ([32]; Fig. 1A, B).…”

Section: Resultsmentioning

confidence: 99%

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The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)

et al. 2013

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A knock-in (KI) mouse model of FHM-1 expressing the R192Q missense mutation of the Cacna1a gene coding for the α1 subunit of CaV2.1 channels shows, at the level of the trigeminal ganglion, selective functional up-regulation of ATP -gated P2X3 receptors of sensory neurons that convey nociceptive signals to the brainstem. Why P2X3 receptors are constitutively more responsive, however, remains unclear as their membrane expression and TRPV1 nociceptor activity are the same as in wildtype (WT) neurons. Using primary cultures of WT or KI trigeminal ganglia, we investigated whether soluble compounds that may contribute to initiating (or maintaining) migraine attacks, such as TNFα, CGRP, and BDNF, might be responsible for increasing P2X3 receptor responses. Exogenous application of TNFα potentiated P2X3 receptor-mediated currents of WT but not of KI neurons, most of which expressed both the P2X3 receptor and the TNFα receptor TNFR2. However, sustained TNFα neutralization failed to change WT or KI P2X3 receptor currents. This suggests that endogenous TNFα does not regulate P2X3 receptor responses. Nonetheless, on cultures made from both genotypes, exogenous TNFα enhanced TRPV1 receptor-mediated currents expressed by a few neurons, suggesting transient amplification of TRPV1 nociceptor responses. CGRP increased P2X3 receptor currents only in WT cultures, although prolonged CGRP receptor antagonism or BDNF neutralization reduced KI currents to WT levels. Our data suggest that, in KI trigeminal ganglion cultures, constitutive up-regulation of P2X3 receptors probably is already maximal and is apparently contributed by basal CGRP and BDNF levels, thereby rendering these neurons more responsive to extracellular ATP.

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Section: Discussionmentioning

confidence: 81%

Section: Resultsmentioning

confidence: 99%

The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)

et al. 2013

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“…93 The pain associated with migraine headache has been hypothesized to be caused by PGE 2, 94 and thus related to increased AA metabolism, 95 as well as increased neuroinflammation in general. 96–98 Both BD and migraine headache respond to several of the same medications, including valproic acid 99,100 and lamotrigine, 101 indicating a potential shared pathology.…”

Section: The Way Forward: Lessons From Migrainementioning

confidence: 99%

Reconsidering Dietary Polyunsaturated Fatty Acids in Bipolar Disorder: A Translational Picture

Saunders

Ramsden

Sherazy

et al. 2016

J. Clin. Psychiatry

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Inflammation is an important mediator of pathophysiology in bipolar disorder (BD). The omega (n)-3 and omega (n)-6 polyunsaturated fatty acid (PUFA) metabolic pathways participate in several inflammatory processes, and have been linked through epidemiological and clinical studies to BD and its response to treatment. We review the proposed role of PUFA metabolism in neuroinflammation, modulation of brain PUFA metabolism by antimanic medications in rodent models, and anti-inflammatory pharmacotherapy in BD and in major depressive disorder (MDD). Though the convergence of findings between pre-clinical and post-mortem clinical data is compelling, we investigate why human trials of PUFA as treatment are mixed. We view the biomarker and treatment study findings in light of the evidence for the hypothesis that arachidonic acid (AA) hypermetabolism contributes to BD pathophysiology, and propose that a combined high n-3 plus low n-6 diet should be tested as an adjunct to current medication in future trials.

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“…Headache is a disabling neurologic condition that affects a considerable amount of the general population and is accompanied with phonophobia, nausea and vomiting [ 2 , 3 ]. Headache occurs in migraines, tension-type headaches, and cluster headaches [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Metabolomics Strategy Using High Resolution Mass Spectrometry Reveals Novel Biomarkers and Pain-Relief Effect of Traditional Chinese Medicine Prescription Wu-Zhu-Yu Decoction Acting on Headache Modelling Rats

Liu

Zhang³

et al. 2017

Molecules

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Headache is a common episodic or chronic neurologic disorder. Treatment options and diagnosis are restricted by an incomplete understanding of disease pathology and the lack of diagnostic markers. Wu-Zhu-Yu decoction (WZYD), a traditional Chinese medicine (TCM) formula containing four TCM herbs, is commonly used in the treatment of headache in China. To deeply understand more about headache and investigate the pain-relief mechanism of WZYD, a comprehensive metabolomics study combined with multivariate data processing strategy was carried out. An LC-high resolution mass spectrometry-based metabolomics approach was applied to characterize metabolic biomarker candidates. Multiple pattern recognition including principal component analysis-discriminant analysis, partial least squares-discriminant analysis and hierarchical cluster analysis were used to determine groups and confirm important variables. A total of 17 potential biomarkers were characterized and related metabolic pathways were identified. The study demonstrated that the established metabolomics strategy is a powerful approach for investigating the mechanism of headache attack and WZYD. In addition, the approach may highlight biomarkers and metabolic pathways and can capture subtle metabolite changes from headache, which may lead to an improved mechanism understanding of central nervous system diseases and TCM treatment.

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Migraine

Cited by 11 publications

References 102 publications

The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)

The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)

Reconsidering Dietary Polyunsaturated Fatty Acids in Bipolar Disorder: A Translational Picture

Metabolomics Strategy Using High Resolution Mass Spectrometry Reveals Novel Biomarkers and Pain-Relief Effect of Traditional Chinese Medicine Prescription Wu-Zhu-Yu Decoction Acting on Headache Modelling Rats

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