Could glial activation be a factor in migraine?
Migraine represents a central neural hypersensitivity. During an attack, migraine sufferers can be hypersensitive to normal levels of sound, light, smell and movement. Sensory processing dysfunction in the brain stem or diencephalic nuclei has been implicated. Most scientific migraine research has focused on neuronal function because of their central role in the processing, integration and transmission of sensory information. However the supporting glia, their receptors and their secreted mediators are now recognised as having an important role in neuronal function regulation. Activated microglia and astrocytes produce and release a variety of neuroexcitatory substances including nitric oxide, excitatory amino acids and proinflammatory cytokines. Spinal glial activation and the subsequent release of proinflammatory mediators initiate and maintain a range of enhanced pain states. The focus on neuronal function has ignored the potential contribution of glial cell activation to neural hypersensitivity and pain. If the central neuronal hypersensitivity associated with migraine represents glial cell activation, drugs that block glial cell activation and the subsequent release of neuroexcitatory substances could have therapeutic potential in both acute migraine treatment and migraine prophylaxis.
Bartley
Jim
J
The Auckland Regional Pain Service, Auckland District Health Board, 10 Owens Road, Epsom, Auckland 1023, New Zealand. jbartley@ihug.co.nz
D001921:Brain / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D051525:Fibroblast Growth Factor 9 / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D008881:Migraine Disorders / Q000188:drug therapy / Q000378:metabolism*; D008959:Models, Neurological; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*
D016207:Cytokines; D051525:Fibroblast Growth Factor 9; D018836:Inflammation Mediators