抄録
The effect of zinc on glycinergic postsynaptic currents (sIPSCs) was studied by using the whole-cell patch-clamp technique in mechanically dissociated rat spinal dorsal horn neurons. Zinc reversibly and concentration-dependently increased sIPSC frequency. Low concentration of zinc potentiated the sIPSC amplitude, while high concentration of zinc inhibited the amplitude. The zinc-induced synaptic potentiation was abolished in the absence of extracellular Ca2+ or by the addition of Cd2+, suggesting the involvement of Ca2+ influx into the nerve terminals. The zinc action was also inhibited in the presence of tetrodotoxin, suggesting that zinc causes depolarization of the nerve terminals. In the slice preparation, zinc potentiated the evoked IPSC amplitude and decreased the paired pulse ratio. These results suggest zinc modulates glycinergic transmission in the spinal cord and plays an important role in the pain transmission. [J Physiol Sci. 2007;57 Suppl:S147]
