The biology of the glutamatergic system and potential role in migraine
Gasparini, Claudia F. & Griffiths, Lyn R. (2013) The biology of the glutamatergic system and potential role in migraine. International Journal of Biomedical Science, 9(1), pp. 1-8.
Migraine is a common genetically linked neurovascular disorder. Approximately ~12% of the Caucasian population are affected including 18% of adult women and 6% of adult men (1, 2). A notable female bias is observed in migraine prevalence studies with females affected ~3 times more than males and is credited to differences in hormone levels arising from reproductive achievements. Migraine is extremely debilitating with wide-ranging socioeconomic impact significantly affecting people's health and quality of life. A number of neurotransmitter systems have been implicated in migraine, the most studied include the serotonergic and dopaminergic systems. Extensive genetic research has been carried out to identify genetic variants that may alter the activity of a number of genes involved in synthesis and transport of neurotransmitters of these systems. The biology of the Glutamatergic system in migraine is the least studied however there is mounting evidence that its constituents could contribute to migraine. The discovery of antagonists that selectively block glutamate receptors has enabled studies on the physiologic role of glutamate, on one hand, and opened new perspectives pertaining to the potential therapeutic applications of glutamate receptor antagonists in diverse neurologic diseases. In this brief review, we discuss the biology of the Glutamatergic system in migraine outlining recent findings that support a role for altered Glutamatergic neurotransmission from biochemical and genetic studies in the manifestation of migraine and the implications of this on migraine treatment.
Impact and interest:
Citation counts are sourced monthly from and citation databases.
These databases contain citations from different subsets of available publications and different time periods and thus the citation count from each is usually different. Some works are not in either database and no count is displayed. Scopus includes citations from articles published in 1996 onwards, and Web of Science® generally from 1980 onwards.
Citations counts from theindexing service can be viewed at the linked Google Scholar™ search.
Full-text downloads displays the total number of times this work’s files (e.g., a PDF) have been downloaded from QUT ePrints as well as the number of downloads in the previous 365 days. The count includes downloads for all files if a work has more than one.
|Item Type:||Journal Article|
|Keywords:||Excitotoxicity, Familial hemiplegic migraine, Glutamate, Migraine with aura, Migraine without aura, Neurotransmitters, Receptors, Transporters, 4 aminobutyric acid, adx 10059, AMPA receptor, anticonvulsive agent, antimigraine agent, beta adrenergic receptor blocking agent, calcium channel blocking agent, excitatory amino acid transporter 1, excitatory amino acid transporter 2, glutamate receptor, glutamic acid, kainic acid receptor, ketamine, memantine, n methyl dextro aspartic acid receptor, sodium channel Nav1.1, topiramate, tricyclic antidepressant agent, unclassified drug, amino acid transport, ataxia, ATP1A2 gene, CACNA1A gene, central nervous system, crystal structure, disease activity, drug mechanism, excitatory amino acid transporter 1 gene, excitatory amino acid transporter 2 gene, excitotoxicity, familial hemiplegic migraine, gene, gene expression regulation, genetic association, genetic linkage, genetic risk, genetic variability, glutamatergic system, Gria1 gene, GRIA3 gene, human, KCNK18 gene, migraine, missense mutation, mutational analysis, nerve cell necrosis, nerve excitability, neuropathology, neuroprotection, neurotransmission, nonhuman, review, RNA editing, SCN1A gene, single nucleotide polymorphism|
|Divisions:||Current > Institutes > Institute of Health and Biomedical Innovation|
|Copyright Owner:||Copyright 2013 the authors|
|Copyright Statement:||This is an open-access article distributed under the
terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/2.5/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
|Deposited On:||27 Sep 2013 04:51|
|Last Modified:||30 Oct 2013 01:14|
Repository Staff Only: item control page