Epidural glutamate excresesnce from disc material causes focal hyperalgesia Academic Article uri icon



    Blinded animal study.


    To determine if an increased concentration of epiduralglutamate can cause a focal nociceptive response in the lower extremities that is consistent with sciatica.


    It is believed that the origin of sciatic pain is related to more than physical pressure on the nerve roots. Recently, it was determined that discmaterial may be a significant source of free glutamate, resulting from the enzymatic degradation of matrix aggrecan proteins. We believe that this free glutamate acts as a neurotransmitter at glutamate receptors on the dorsal root ganglion (DRG) cell bodies, thereby initiating a nociceptive response.


    Rats were subject to a 72-hour epiduralglutamate infusion via a mini osmotic pump. Von Frey behavioral testing was performed 24 hours before, and 24 and 72 hours after the onset of the infusion. DRG and dorsal horn tissues were analyzed for changes in receptor expression, which have been previously shown to correlate with a nociceptive state.


    Von Frey behavioral tests showed focalhyperalgesia that was maximal at the 0.02 mmol/L glutamate concentration. Significant changes in DRG glutamate receptor expression were seen for alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid, kainite, and N-methyl-D aspartate receptors. Analysis of dorsal horn glutamate receptors also showed patterns in alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid and kainate receptor expression that were consistent with a nociceptive state.


    Epiduralglutamate elicits a focal nociceptive response. Free glutamate that has been liberated from the discmaterial may be an important factor in the development of sciatic pain.

    PMID: 15770173 [PubMed - indexed for MEDLINE]

publication date

  • January 1, 2010