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The role of monosodium glutamate in headache O'Brien, Melissa


Consumption of monosodium glutamate (MSG) can induce headache in young healthy individuals and migraine-like headache in migraineurs. Blood plasma levels of glutamate are also elevated in migraineurs, but it is unknown how elevated levels of glutamate contribute to headache. The current study was undertaken to investigate the hypothesis that monosodium glutamate induces headache through activation of peripheral glutamate receptors. To test the hypothesis, we combined in vivo electrophysiology, laser Doppler recordings of dural vasculature, and immunohistochemistry to investigate the effect of systemic administration of MSG on the trigeminovascular pathway. Immunohistochemical analysis of the dura, determined that the nerve fibres innervating dural blood vessels express NMDA, AMPA, kainate and mGlur5 receptors. The glutamate transporter EAAT2, but not EAAT1 or 3, is expressed by dural blood vessels. Systemic administration of 50mg/kg MSG induced a 24.5 and 20.6 percent increase in dural blood flow in male and female rats, respectively, as measured by laser Doppler flowmetry. Dural blood flow returned to baseline values by a mean of 170 seconds. In in vivo extracellular recordings of spinal trigeminal subnucleus caudalis (SpVc) neurons with dural receptive fields, intravenously administered MSG evoked an increase in neuronal discharge in 5/6 neurons in both male and female rats. MSG also induced mechanical sensitization in both sexes. When the NMDA receptor selective antagonist APV (5, 50mg/kg) was co-administered with MSG, it attenuated both the MSG evoked activation and mechanical sensitization of SpVc neurons. My results suggest that MSG induced headache is mediated, in part, through activation of the peripheral NMDA receptor.

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