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首页> 外文期刊>The European Journal of Neuroscience >Taurine potentiates presynaptic NMDA receptors in hippocampal Schaffer collateral axons.
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Taurine potentiates presynaptic NMDA receptors in hippocampal Schaffer collateral axons.

机译：牛磺酸增强海马Schaffer侧支轴突突触前NMDA受体。

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摘要

We have previously shown that activation of presynaptic N-methyl-d-aspartate (NMDA) receptors (NMDAR) enhances the amplitude of the presynaptic fibre volley (FV) evoked in Schaffer collateral axons of rat hippocampal slices, by a mechanism independent of extracellular Ca(2+). Here we compared the pharmacological characteristics of presynaptic NMDARs affecting axon excitability (activated by 10-300 microM NMDA for 10 min), with those mediating field excitatory postsynaptic potentials (NMDA-fEPSP). We found that NMDA-induced potentiation was completely inhibited by NVP-AAM077, an antagonist of NR2A-containing NMDAR, but not by ifenprodil, an NR2B-selective antagonist. The inhibitor of the glycine-binding site in NMDARs, 7-clorokynurenic acid (7-CK), was more potent against NMDA-fEPSP (IC(50) = 6.3 +/- 1.3 microM) than against the NMDA-induced FV potentiation (IC(50) = 26.5 +/- 1.3 microM). Moreover, both post- and presynaptic NMDAR-mediated phenomena were enhanced by glycine and d-serine, but taurine, anendogenous analogue of glycine, only enhanced the latter (EC(50) = 19 microM). Taurine was able to block the inhibitory effect of low doses of 7-CK on NMDA-induced FV potentiation, while glycine and d-serine only reduced the effects of higher concentrations of this drug. Surprisingly, the enhancing effect of taurine on NMDA-induced FV potentiation was blocked when it was co-applied with glycine. Furthermore, the glutamate released synaptically with a train of stimuli also increased FV amplitude by a mechanism dependent on NMDARs; this was potentiated by taurine but not by co-application of taurine and glycine. These results reveal that presynaptic NMDARs have unique properties that mediate the facilitation of axon excitability.
机译：先前我们已经表明，通过独立于细胞外Ca的机制，激活突触前N-甲基-d-天冬氨酸（NMDA）受体（NMDAR）可以增强大鼠海马切片Schaffer侧突轴突中诱发的突触前纤维齐射（FV）的幅度。 （2+）。在这里，我们比较了影响轴突兴奋性（由10-300 microM NMDA激活10分钟）的突触前NMDAR的药理学特征与介导现场兴奋性突触后电位（NMDA-fEPSP）的药理学特征。我们发现NMDA诱导的增强作用被NVP-AAM077（一种含NR2A的NMDAR的拮抗剂）完全抑制，但未被艾芬地尔（一种NR2B选择性拮抗剂）完全抑制。 NMDAR中甘氨酸结合位点的抑制剂7-氯尿酸（7-CK）对NMDA-fEPSP（IC（50）= 6.3 +/- 1.3 microM）比对NMDA诱导的FV增强更有效（ IC（50）= 26.5 +/- 1.3 microM）。此外，甘氨酸和d-丝氨酸增强了突触后和突触前NMDAR介导的现象，但是牛磺酸（甘氨酸的内源性类似物）仅增强了后者（EC（50）= 19 microM）。牛磺酸能够阻断低剂量的7-CK对NMDA诱导的FV增强的抑制作用，而甘氨酸和d-丝氨酸只能降低较高浓度的该药物的作用。令人惊讶的是，当牛磺酸与甘氨酸共同使用时，牛磺酸对NMDA诱导的FV增强的增强作用被阻断。此外，通过一系列刺激突触释放的谷氨酸盐也通过依赖于NMDAR的机制增加了FV振幅。牛磺酸可增强这种作用，但牛磺酸和甘氨酸不能同时使用。这些结果表明突触前NMDARs具有独特的属性，介导轴突兴奋性的促进。

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