Effect of inhibition of spinal cord glutamate transporters on inflammatory pain induced by formalin and complete Freund's adjuvant.

摘要: BACKGROUND Spinal cord glutamate transporters clear synaptically released and maintain normal sensory transmission. However, their ultrastructural localization is unknown. Moreover, whether how they participate in inflammatory pain has not been carefully studied. METHODS Immunogold labeling with electron microscopy was carried out to characterize synaptic nonsynaptic of the superficial dorsal horn. Their expression uptake activity after formalin- complete Freund's adjuvant (CFA)-induced inflammation were evaluated by Western blot analysis assay. Effects intrathecal transporter activator (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline inhibitors (DL-threo-β-benzyloxyaspartate [TBOA], dihydrokainate, DL-threo-β-hydroxyaspartate), or TBOA plus group III metabotropic receptor antagonist (RS)-α-methylserine-O-phosphate, on CFA-induced examined. RESULTS In horn, excitatory amino acid carrier 1 localized presynaptic membrane, postsynaptic axonal dendritic membranes at sites, whereas transporter-1 glutamate/aspartate are prominent glial membranes. Although these three spinal altered h formalin injection 6 CFA injection, decreased time points. Intrathecal had no effect formalin-induced behaviors. contrast, TBOA, DL-threo-β-hydroxyaspartate reduced formalin-evoked behaviors second phase. also attenuated thermal hyperalgesia injection. The antinociceptive effects blocked coadministration (RS)-α-methylserine-O-phosphate. CONCLUSION Our findings suggest that inhibition relieves through activation inhibitory receptors.