Differential regulation of glutamate receptors in trigeminal ganglia following masseter inflammation.

The present study examined whether N-methyl-D-aspartate receptor (NMDAR), 5-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits and group I metabotropic glutamate receptors (mGluRs) are constitutively expressed in trigeminal ganglia (TG) using Western blot analysis in male Sprague-Dawley rats. We then investigated whether experimental induction of masseter inflammation influences glutamate receptor expressions by comparing the protein levels from naïve rats to those from complete Freund's adjuvant (CFA) inflamed rats. Our results showed that NMDAR1 (NR1), NMDAR2A (NR2A), NMDAR2B (NR2B), AMPAR1 (GluR1) and AMPAR2 (GluR2) subunits, and group I metabotropic glutamate receptor, mGluR5, are constitutively expressed in TG. Masseter inflammation significantly down-regulated NR1 subunit expression that persisted to 7 days post-CFA inflammation. NR2A and NR2B expressions were not significantly changed. GluR1 receptor subunit expression was slightly increased in TG 3 days after CFA-induced inflammation, but the change was not statistically significant. GluR2 protein level was not affected by CFA inflammation. The level of mGluR5 protein was significantly up-regulated in TG 3 days after CFA-induced masseter inflammation. There were no inflammation-induced changes in any of the proteins we analyzed in the contralateral, non-inflamed TG. These results suggested that muscle inflammation differentially modulates glutamate receptor subunits at the primary afferent level in male rats and that these inflammation-induced transcriptional changes may contribute to functionally different aspects of craniofacial muscle pain.