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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide
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Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide

机译：抗坏血酸作为下丘脑的抑制性递质，通过清除一氧化氮来抑制刺激的促黄体生成素释放激素释放

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摘要

Because ascorbic acid (AA) is concentrated in synaptic vesicles con- taining glutamic acid, we hypothesized that AA might act as a neurotransmitter. Because AA is an antioxidant, it might therefore inhibit nitric oxidergic (NOergic) adivation of luteinizing hormone- releasing hormone (LH-RH) release from medial basal hypothalamic explants by chemically reducing NO. Cell membrane depolarization induced by increased pot8ssium concentration [K+] increased me- dium concentrations of both AA and LH-RH. An inhibitor of NO synthase (NOS), NG-monomethyl-L-arginine (NMMA), prevented the increase in medium concentrations of AA and LH-RH induced by high [K+], suggesting that NO mediates release of both AA and LH-RH. Calcium-free medium blocked not only the increase in AA in the medium but also the release of LH-RH. Sodium nitroprusside. which releases NO, Stimulated LH-RH release and decreased the concentra- tion of AA in the incubation medium. presumably because the NO released oxidized AA to dehydro-AA. AA (10--5 to 10--3 M) had no effect on basal LH-RH release but completely blocked high [K+]- and nitroprusside-induced LH-RH release. NMethyl-D-aspartic acid (NMDA). which mimics the action of the excitatory amino acid neu- rotransmitt6r glutamic acid, releases LH-RH by releasing NO. AA (10--s to 10--s M) inhibited the LH-RH-releasing action of NMDA. AA may be an inhibitory neurotransmitter that blocks Noergic stimulation of LH-RH release by chemically reducing the NO released by the Noergic neurons.
机译：因为抗坏血酸（AA）集中在含有谷氨酸的突触小泡中，所以我们假设AA可能是神经递质。由于AA是抗氧化剂，因此它可能通过化学还原NO来抑制从内侧下丘脑外植体释放的黄体生成激素释放激素（LH-RH）的一氧化氮（NOergic）增殖。钾浓度[K +]升高引起的细胞膜去极化作用，AA和LH-RH的培养基浓度均升高。 NO合酶（NOS）抑制剂NG-单甲基-L-精氨酸（NMMA）阻止了高[K +]诱导的AA和LH-RH中等浓度的增加，表明NO介导了AA和LH-两者的释放。 RH。无钙培养基不仅阻止培养基中AA的增加，而且阻止LH-RH的释放。硝普钠。释放NO，刺激LH-RH释放，并降低培养液中AA的浓度。大概是因为NO释放了氧化的AA到脱氢AA。 AA（10--5至10--3 M）对基础LH-RH的释放没有影响，但完全阻止了高[K +]-和硝普钠诱导的LH-RH的释放。 NMethyl-D-天冬氨酸（NMDA）。模仿兴奋性氨基酸神经递质谷氨酸的作用，通过释放NO释放LH-RH。 AA（10--s至10--s M）抑制NMDA的LH-RH释放作用。 AA可能是一种抑制性神经递质，可通过化学还原Noergic神经元释放的NO来阻止LH-RH释放的Noergic刺激。

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