Inflammation-induced upregulation of AMPA receptor subunit expression in brain stem pain modulatory circuitry.

Our previous study demonstrated an increase in alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor sensitivity in the rostral ventromedial medulla (RVM) associated with enhanced net descending inhibition after inflammatory hyperalgesia. The present study further studied the time-dependent changes in AMPA-produced inhibition after inflammation and the underlying molecular mechanisms. Inflammation was induced by intraplantar injection of complete Freund's adjuvant (CFA, 0.

Tyrosine phosphorylation of the NR2B subunit of the NMDA receptor in the spinal cord during the development and maintenance of inflammatory hyperalgesia.

The present study examined the levels of NMDA receptor NR2 subunit tyrosine phosphorylation in a rat model of inflammation and correlated it with the development of inflammation and hyperalgesia. Hindpaw inflammation and hyperalgesia were induced by intraplantar injection of complete Freund's adjuvant. Proteins from the spinal cord (L4-L5) were immunoprecipitated with anti-NR2A or anti-NR2B antibodies and used for subsequent analysis using 4G-10, a specific anti-phosphotyrosine antibody.

Plasticity in excitatory amino acid receptor-mediated descending pain modulation after inflammation.

The role for excitatory amino acids (EAAs) in the rostral ventromedial medulla (RVM) in descending pain modulation after persistent noxious input is unclear. In an animal model of inflammatory hyperalgesia, we examined the effects of intra-RVM microinjection of EAA receptor agonists and antagonists on paw withdrawal and tail-flick responses in lightly anesthetized rats. N-Methyl-D-aspartate (NMDA) produced effects that depended upon the postinflammatory time period.