OBJECTIVE To investigate effects of oxymatrine,an alkaloid from Sophora flavescens Ait.,on high-voltage dependent calcium channel and inhibitory neurotransmitter GABA under neuropathic pain condition.METHODS The partial sciatic nerve ligation(PSNL)was executed on C57/BL6 mice to produce neuropathic pain.Oxymatrine(150 mg·kg-1)was administrated intraperitoneally to PSNL mice.Mechanical hindpaw withdral threshold(MWT)was measured under Von-Frey filament stimulation with up-and-down method.In brain tissue,GABA concentration was measured with ELISA.Change of GABAAreceptor protein expression,N-type calcium channel(Cav2.2)and L-type calcium channel(Cav1.3)protein expressions were detected with Western-blot;intracellular calcium concentration was measured in cultured cortical neurons with Fluo-3/AM fluorescent probe.RESULTS Compared to saline,oxymatrine significantly increased ED50 of MWT on PSNL mice(P<0.05).GABA concentration and GABAAreceptor protein level in brain tissue were decreased in PSNL mice,while administration of oxymatrine increased both GABA concentration and GABAA receptor expression.Intracellular calcium concentration was increased in cultured cortical neurons by oxymatrine treatment,but this phenomenon was not seen under calcium-free condition.Protein expression of Cav2.2,but not Cav1.3,was found to be decreased in the brains of PSNL mice and to be restored to a normal level with oxymatrine administration.CONCLUSION Oxymatrine has analgesic effect on PSNL-induced neuropathic pain in mice.This phenominon relates to the increase of GABA release,GABAAreceptor expression,and also the restoration of expression level of Cav2.2 but not Cav1.3 in brain tissues,which suggesting that Ca2+ flow through Cav2.2 calcium channel may be the key point underlying oxymatrine analgesia. OBJECTIVE To investigate effects of oxymatrine, an alkaloid from Sophora flavescens Ait., On high-voltage dependent calcium channel and inhibitory neurotransmitter GABA under neuropathic pain condition. METHODS The partial sciatic nerve ligation (PSNL) was executed on C57 / BL6 mice to produce neuropathic pain and oxytocin (150 mg · kg-1) was administrated intraperitoneally to PSNL mice. Mechanical and mechanical measures were measured with Von- ELISA. Change of GABAA receptor protein expression, N-type calcium channel (Cav2.2) and L-type calcium channel (Cav1.3) protein expressions were detected with Western-blot; intracellular calcium concentration was measured in cultured cortical neurons with Fluo- 3 / AM fluorescent probe. RESULTS Compared to saline, oxymatrine significantly increased ED50 of MWT on PSNL mice (P <0.05) .GABA concentration and GABAA receptor protein level in brain tissue were decreased i n PSNL mice, while administration of oxymatrine increased both GABA concentration and GABAA receptor expression. Intracellular calcium concentration was increased in cultured cortical neurons by oxymatrine treatment, but this phenomenon was not seen under calcium-free condition. Protein expression of Cav2.2, but not Cav1.3, was found to be decreased in the brains of PSNL mice and to be restored to a normal level with oxymatrine administration. CONCLUSION Oxymatrine has analgesic effect on PSNL-induced neuropathic pain in mice. This phenominon relates to the increase of GABA release, GABAAreceptor expression, and also the restoration of expression level of Cav2.2 but not Cav1.3 in brain tissues, which suggests that Ca2 + flow through Cav2.2 calcium channel may be the key point underlying oxymatrine analgesia.