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摘要Gentiopicroside is one of the secoiridoid compound isolated from Gentiana lutea. It exhibits analgesicactivities in the mice. The anterior cingulate cortex（ACC) is a f-orebrain structure known for its rolesin pain transmission and modulation. Painful stimuli potentiate the prefrontal synaptic transmissionand induce glutamate NMDA NR2Breceptor expression in the ACC. But little is known aboutGentiopicroside on the per-sistent inflammatory pain and chronic pain-induced synaptic transmissionchanges in the ACC. The present study was undertaken to investigate its analgesic activities andcentral synaptic modulation to the peripheral painful inflammation. Gentiopicrosideproducedsignificant analgesic effects against persistent inflammatory pain stimuli i-n mice. Systemicadministration of Gentiopicroside significantly reversed NR2B over-expression during the chronicphases of persistent inflammation caused by hind-paw ad-ministration of complete Freunds adjuvant(CFA) in mice. Whole-cell patch-clamp reco-rdings revealed that Gentiopicroside significantlyreduced NR2B receptors mediated p-ostsynaptic currents in the ACC. Our findings provide strongevidence that analgesiceffects of Gentiopicroside involve down-regulation of NR2B receptors in theACC to persistent inflammatory pain.