The effect of zinc on glycinergic inhibitory postsynaptic currents in rat spinal dorsal horn neurons
The effect of zinc on glycinergic inhibitory postsynaptic currents in rat spinal dorsal horn neurons
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DOI：
10.1016/j.brainres.2007.05.060
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发表时间：
2007-08-03
期刊：
影响因子：
2.9
通讯作者：
Ishibashi, Hitoshi
中科院分区：
文献类型：
--
作者：
Eto, Kei;Arimura, Yukiko;Ishibashi, Hitoshi
在机械分离的大鼠脊髓背角神经元上，用全细胞膜片钳技术研究了锌对甘氨酸能自发抑制性突触后电流（IPSCs）的影响。锌在10 μ M的浓度可逆地增加了自发IPSC的频率，而不改变电流的幅度，这表明锌增加自发的甘氨酸释放突触前神经末梢。另一方面，在1 μ M的低浓度下，锌增强自发IPSC的振幅，但对频率没有影响。在100 μ M的高浓度下，锌增加了自发IPSC频率，同时抑制了IPSC振幅。外源性甘氨酸诱发的电流分别被低浓度和高浓度的锌增强和抑制。在ω-芋螺毒素-MVIIC和硝苯地平存在下，通过阻断电压依赖性Ca 2+通道，10 μ M锌引起的自发IPSC频率的增加被抑制。在河豚毒素的存在下，锌对自发IPSC频率的易化作用也被抑制。在切片制备中，30 μ M锌增强诱发的IPSC振幅，降低成对脉冲比。这些结果表明，除了对突触后甘氨酸受体的作用外，锌还可以使突触前神经末梢去极化，导致电压依赖性Na+和Ca 2+通道的激活，这反过来又增加甘氨酸的释放。由于背角神经元接受伤害性信息，锌可能在感觉传递的调节中发挥重要作用。
The effect of zinc on glycineygic spontaneous inhibitory postsynaptic cur-rents (IPSCs) was investigated using the whole-cell patch-clamp technique in mechanically dissociated rat spinal dorsal horn neurons. Zinc at a concentration of 10 mu M reversibly increased the spontaneous IPSC frequency without changing the current amplitudes, suggesting that zinc increases spontaneous glycine release from presynaptic nerve terminals. At a low concentration of 1 mu M, on the other hand, zinc potentiated the amplitude of spontaneous IPSCs but had no effect on the frequency. At a high concentration of 100 mu M, zinc increased the spontaneous IPSC frequency while it inhibited the IPSC amplitude. The current evoked by exogenously applied glycine was potentiated and inhibited by low and high concentrations of zinc, respectively. The increase in spontaneous IPSC frequency by 10 mu M zinc was inhibited by blocking the voltage -dependent Ca2+ channels in the presence of both omega-conotoxin-MVIIC and nifedipine. The facilitatory effect of zinc on spontaneous IPSC frequency was also inhibited in the presence of tetrodotoxin. In the slice preparation, 30 mu M zinc potentiated the evoked IPSC amplitude and decreased the paired pulse ratio. These results suggest that, in addition to an action on the postsynaptic glycine receptors, zinc may depolarize the presynaptic nerve terminals, leading to an activation of voltage - dependent Na+ and Ca2+ channels that in turn increases glycine release. Since dorsal horn neurons receive nociceptive inputs, zinc may play an important role in the regulation of sensory transmission.