Down-regulation of NR2B receptors partially contributes to analgesic

Chen Lei; Sun Wenji; Zhao Minggao

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Down-regulation of NR2B receptors partially contributes to analgesic

Chen Lei 1,Sun Wenji 1 #,Zhao Minggao 2 *

1.Department of Chinese Traditional Medicine, College of Life Science, Northwest University

2.Department of Pharmacology, School of Pharmacy, Fourth Military Medical University

*Correspondence author

#Submitted by

Subject:

Funding: 高等学校博士学科点专项科研基金（No.20060697014）

Opened online:17 March 2010

Accepted by: none

Citation: Chen Lei ,Sun Wenji ,Zhao Minggao .Down-regulation of NR2B receptors partially contributes to analgesic[OL]. [17 March 2010] http://en.paper.edu.cn/en_releasepaper/content/40796

Gentiopicroside is one of the secoiridoid compound isolated from Gentiana lutea. It exhibits analgesic activities in the mice. The anterior cingulate cortex (ACC) is a forebrain structure known for its roles in pain transmission and modulation. Painful stimuli potentiate the prefrontal synaptic transmission and induce glutamate NMDA NR2B receptor expression in the ACC. But little is known about Gentiopicroside on the persistent inﬂammatory pain and chronic pain-induced synaptic transmission changes in the ACC. The present study was undertaken to investigate its analgesic activities and central synaptic modulation to the peripheral painful inﬂammation. Gentiopicroside produced signiﬁcant analgesic effects against persistent inﬂammatory pain stimuli in mice. Systemic administration of Gentiopicroside signiﬁcantly reversed NR2B over-expression during the chronic phases of persistent inﬂammation caused by hind-paw administration of complete Freunds adjuvant (CFA) in mice. Whole-cell patch clamp recordings revealed that Gentiopicroside signiﬁcantly reduced NR2B receptors mediated postsynaptic currents in the ACC. Our ﬁndings provide strong evidence that analgesic effects of Gentiopicroside involve down-regulation of NR2B receptors in the ACC to persistent inﬂammatory pain.

Keywords:Gentiopicroside;Inﬂammation;Pain;NMDA receptor;Anterior cingulate cortex

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