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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Nitric oxide-independent inhibition by sodium nitroprusside of the native N-methyl-D-aspartate recognition domain in a manner different from that by potassium ferrocyanide.
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Nitric oxide-independent inhibition by sodium nitroprusside of the native N-methyl-D-aspartate recognition domain in a manner different from that by potassium ferrocyanide.

机译：硝普钠对天然N-甲基-D-天冬氨酸识别域的一氧化氮非依赖性抑制作用，其方式不同于亚铁氰化钾。

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摘要

Binding of [3H](+)-5-methyl-10,11 -dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) was significantly inhibited by the addition of sodium nitroprusside (SNP), a nitric oxide (NO) donor, at a concentration range of 0.1 microM to 0.1 mM in rat brain synaptic membranes. On the contrary, two other NO donors, S-nitroso-N-acetylpenicillamine and S-nitroso-L-glutathione, did not inhibit binding even at 0.1 mM. Similarly potent inhibition of [3H]MK-801 binding was caused by the addition of potassium ferrocyanide, while potassium ferricyanide induced slight inhibition of binding at 0.1 mM. Both SNP and potassium ferrocyanide markedly inhibited binding of [3H]glutamic (Glu) and [3H]D,L-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic acids, without significantly affecting that of [3H]glycine and [3H]5,7-dichlorokynurenic acid. Further addition of Glu significantly exacerbated the inhibition by both SNP and potassium ferrocyanide at concentrations of 1-10 microM. Potent inhibition was also induced for [3H]MK-801 binding by the treatment of synaptic membranes with either SNP or potassium ferrocyanide, followed by efficient washing which also inhibited [3H]MK-801 binding due to removal of endogenous agonists. By contrast, dithiothreitol clearly differentiated between inhibitory properties of SNP and potassium ferrocyanide on [3H]MK-801 binding in terms of reversibility of the inhibition following pretreatment and subsequent washing. These results suggest that SNP may interfere with opening processes of the native NMDA channel through molecular mechanisms different from those underlying the inhibition by potassium ferrocyanide at the NMDA recognition domain in a manner independent of the generation of NO radicals.
机译：硝普钠（SNP）显着抑制了[3H]（+）-5-甲基-10,11-二氢-5H-二苯并[a，d]环庚-5,10-亚胺（MK-801）的结合），一氧化氮（NO）供体，在大鼠脑突触膜中的浓度范围为0.1 microM至0.1 mM。相反，另外两个NO供体S-亚硝基-N-乙酰青霉胺和S-亚硝基-L-谷胱甘肽即使在0.1 mM时也不能抑制结合。类似地，通过加入亚铁氰化钾可有效抑制[3H] MK-801的结合，而铁氰化钾在0.1 mM时可引起对结合的轻微抑制。 SNP和亚铁氰化钾均显着抑制[3H]谷氨酸（Glu）和[3H] D，L-（E）-2-氨基-4-丙基-5-膦基-3-戊烯酸的结合，而对SNP和亚铁氰化钾均无明显影响。 [3H]甘氨酸和[3H] 5,7-二氯基尿酸。在1-10 microM的浓度下进一步添加Glu会显着加剧SNP和亚铁氰化钾的抑制作用。还可以通过用SNP或亚铁氰化钾处理突触膜来诱导对[3​​H] MK-801结合的有效抑制，然后进行有效洗涤，由于去除了内源性激动剂，它也抑制了[3H] MK-801的结合。相比之下，就预处理和后续洗涤后的抑制作用的可逆性而言，二硫苏糖醇明显区分了SNP和亚铁氰化钾对[3H] MK-801结合的抑制特性。这些结果表明，SNP可能通过分子机制与NMDA识别域中亚铁氰化钾抑制的潜在分子机制不同，而以独立于NO自由基生成的方式干扰其分子机制。

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