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首页> 外文期刊>The European Journal of Neuroscience >Potentiation of inhibitory glycinergic neurotransmission by Zn2+: a synergistic interplay between presynaptic P2X2 and postsynaptic glycine receptors.
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Potentiation of inhibitory glycinergic neurotransmission by Zn2+: a synergistic interplay between presynaptic P2X2 and postsynaptic glycine receptors.

机译：Zn2 +对抑制性甘氨酸能神经传递的增强作用：突触前P2X2与突触后甘氨酸受体之间的协同相互作用。

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摘要

The divalent cation zinc is known to modulate chloride currents carried by native and recombinant mammalian glycine receptors (GlyRs). To unravel the effect of Zn2+ on glycinergic neurotransmission, inhibitory postsynaptic currents (IPSC) of rat spinal neurons grown in culture were analysed in the absence and presence of Zn2+. Low concentrations of Zn2+ (0.5 and 5 micro m) augmented the mean amplitude of miniature IPSCs by approximately 40% over values obtained in the absence of zinc, whereas higher concentrations of Zn2+ (50 micro m) significantly decreased mean amplitude values. Remarkably, low concentrations of Zn2+ also significantly increased the mean frequency of miniature IPSCs. This effect was blocked by the P2X receptor antagonists PPADS and suramin, indicating the presence of Zn2+-sensitive presynaptic P2X receptors on glycinergic terminals. Immunostaining with antibodies against different P2X receptor subtypes revealed that P2X2 receptors partially colocalize with the GlyR. Potentiating concentrations of Zn2+ also affected the kinetics of miniature and evoked IPSCs by significantly prolonging their decay time constants. Electrophysiological analysis of heterologously expressed glycine transporters (GlyT) revealed for GlyT2 zero, and for GlyT1 a modest (< 20%), reduction of glycine uptake in the presence of 5 micro m Zn2+, indicating that prolongation of glycinergic IPSCs by Zn2+ is not due to inhibition of glycine removal from the synaptic cleft. Together, these results suggest that Zn2+ is a potent modulator of glycinergic synaptic transmission which increases in a synergistic manner the agonist affinity of both presynaptic P2X2 receptors and postsynaptic GlyRs.
机译：已知二价阳离子锌可调节天然和重组哺乳动物甘氨酸受体（GlyRs）携带的氯离子电流。为了揭示Zn2 +对甘氨酸能神经传递的影响，分析了在不存在和存在Zn2 +的情况下培养的大鼠脊髓神经元的抑制性突触后电流（IPSC）。低浓度的Zn2 +（0.5和5微米）比没有锌时获得的值增加了微型IPSC的平均幅度约40％，而较高浓度的Zn2 +（50微米）则显着降低了平均幅度值。值得注意的是，低浓度的Zn2 +也显着增加了微型IPSC的平均频率。该作用被P2X受体拮抗剂PPADS和苏拉明阻断，表明在甘氨酸能末端存在Zn2 +敏感的突触前P2X受体。用针对不同P2X受体亚型的抗体进行免疫染色显示，P2X2受体与GlyR部分共定位。增强浓度的Zn2 +还通过显着延长其衰减时间常数来影响微型和诱发的IPSC的动力学。异源表达的甘氨酸转运蛋白（GlyT）的电生理分析显示，对于GlyT2为零，对于GlyT1为适度（<20％），在5微米Zn2 +存在下甘氨酸吸收减少，这表明不是由于Zn2 +延长了甘氨酸能性IPSC。抑制从突触裂缝中去除甘氨酸。总之，这些结果表明，Zn 2+是强力的突触传递的有效调节剂，其以协同方式增加突触前P2X2受体和突触后GlyRs的激动剂亲和力。

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