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首页> 外文期刊>The European Journal of Neuroscience >Modulation of glycine responses by dihydropyridines and verapamil in rat spinal neurons.
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Modulation of glycine responses by dihydropyridines and verapamil in rat spinal neurons.

机译：二氢吡啶和维拉帕米在大鼠脊髓神经元中对甘氨酸反应的调节。

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摘要

Although glycine receptors (GlyRs) are responsible for the main spinal inhibitory responses in adult vertebrates, in the embryo they have been reported to mediate depolarizing responses, which can sometimes activate dihydropyridine-sensitive L-type calcium channels. However, these channels are not the only targets of dihydropyridines (DHPs), and we questioned whether GlyRs might be directly modulated by DHPs. By whole-cell recording of cultured spinal neurons, we investigated modulation of glycine responses by the calcium channel antagonists, nifedipine, nitrendipine, nicardipine and (R)-Bay K 8644, and by the calcium channel, agonist (S)-Bay K 8644. At concentrations between 1 and 10 microM, all these DHPs could block glycine responses, even in the absence of extracellular Ca2+. The block was stronger at higher glycine concentrations, and increased with time during each glycine application. Nicardipine blocked GABAA responses from the same neurons in a similar manner. In addition to their blocking effects, nitrendipine and nicardipine potentiated the peak responses to low glycine concentrations. Both effects of extracellular nitrendipine on glycine responses persisted when the drug was present in the intracellular solution. Thus, these modulations are related neither to calcium channel modulation nor to possible intracellular effects of DHPs. Another type of calcium antagonist, verapamil (10-50 microM), also blocked glycine responses. Our results suggest that some of the effects of calcium antagonists, including the neuroprotective and anticonvulsant effects of DHPs, might result partly from their interactions with ligand-gated chloride channels.
机译：尽管甘氨酸受体（GlyRs）负责成年脊椎动物的主要脊柱抑制反应，但据报道，它们在胚胎中介导去极化反应，有时可激活对二氢吡啶敏感的L型钙通道。但是，这些通道不是二氢吡啶（DHP）的唯一靶标，我们质疑GlyRs是否可能被DHP直接调节。通过培养的脊髓神经元的全细胞记录，我们研究了钙通道拮抗剂硝苯地平，尼群地平，尼卡地平和（R）-Bay K 8644以及钙通道激动剂（S）-Bay K 8644对甘氨酸反应的调节作用在1到10 microM之间的浓度下，即使没有细胞外Ca2 +，所有这些DHP都能阻断甘氨酸反应。在更高的甘氨酸浓度下，该阻滞作用更强，并且在每次施用甘氨酸的过程中，阻滞随时间增加。尼卡地平以相似的方式阻断了来自相同神经元的GABAA反应。除阻断作用外，尼群地平和尼卡地平还增强了对低甘氨酸浓度的峰值响应。当药物存在于细胞内溶液中时，细胞外硝苯地平对甘氨酸反应的两种作用均持续存在。因此，这些调节既不涉及钙通道调节也不涉及DHP的可能的细胞内作用。另一种钙拮抗剂维拉帕米（10-50 microM）也能阻断甘氨酸反应。我们的结果表明，钙拮抗剂的某些作用，包括DHP的神经保护作用和抗惊厥作用，可能部分是由于它们与配体-门控氯化物通道的相互作用所致。

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