Expression of DRD1 mRNA after Spinal Cord Injury Induced Spasticity in Rats

[Objectives]To investigate the spasticity of rat tail and the expression of dopamine receptor-1(DRD1)mRNA in the spinal cord after spinal cord injury(SCI)induced tail spasticity in rats.[Methods]Adult male Wistar rats were randomly divided into Sham group and SCI group.The second sacral spinal cord(S2)segment of SCI rats was completely transected.60 d after operation,the rat tail spasticity was scored,and then the spinal cord tissues below the level of S2 spinal cord transection were taken.The expression of DRD1 mRNA in the sacrococcygeal spinal cord was detected by qPCR.In addition,3 normal rats were used for DAR/neuronal nuclei(NeuN)and DRD1/choline acetyltransferase(ChAT)immunofluorescence staining to study the distribution of DRD1 in spinal cord and the properties of DRD1 positive cells.[Results]60 d after operation in SCI group,the tail spasticity of rats developed fully,and the symptoms of spasticity were typical.qPCR results showed that the expression of DRD1 mRNA in SCI group was significantly lower than that in Sham group(P<0.05).DRD1 was widely distributed in the dorsal horn,intermediate zone and ventral horn at the sacrococcygeal end of the rat spinal cord.[Conclusions]The decrease of DRD1 mRNA expression after SCI may be related to the occurrence and development of spasticity.

The anti-nociceptive effect of bufalin,an active ingredient from toad venom via modulating voltage-gated sodium channels

OBJECTIVE Toad venom(Venenum Bufonis)isalways used for analgesia in China from ancient to modern times,but the effective component of it remains unclear.METHODS In the present study,we investigated the anti-nociceptive effect and the underlying mechanism ofbufalin,an active ingredient fromtoad venom by animal behavior,patch clamp and calcium imaging.RESULTS Bufalin could significantly relieve formalin-induced spontaneous flinching and licking response as well as carrageenan-induced mechanical and thermal hyperalgesia.Using the whole-cel patch-clamp recording,bufalincaused remarkable suppressive effect on the peak currents of Na+channels in dorsal root ganglion neuroblastoma ND7-23 cel line in a U-shaped dependent manner.In addition,bufalinprompted the voltage-dependent activationand caused a negative shift of the fast-state inactivation of Na+channels.However,bufalin produced insignificant effect not onlyon voltage-dependent Kv4.2,Kv4.3 and BK channels,but also on the capsaicin induced Ca2+influx.CONCLUSION The present results indicate bufalin is capable of producing remarkable anti-nociceptive effects whichis probably ascribed to its specific modulation of voltage-gated Na+channels.