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Interaction of PGHS-2 and glutamatergic mechanisms controlling the ovine fetal hypothalamus-pituitary-adrenal axis

机译：PGHS-2与控制绵羊胎儿下丘脑-垂体-肾上腺轴的谷氨酸能机制的相互作用

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Prostaglandins, generated within the fetal brain, are integral components of the mechanism controlling the fetal hypothalamus-pituitary-adrenal (HPA) axis. Previous studies in this laboratory demonstrated that prostaglandin G/H synthase isozyme 2 (PGHS-2) inhibition reduces the fetal HPA axis response to cerebral hypoperfusion, blocks the preparturient rise in fetal plasma ACTH concentration, and delays parturition. We also discovered that blockade of N-methyl-d-aspartate (NMDA) receptors reduces the fetal ACTH response to cerebral hypoperfusion. The present study was designed to test the hypothesis that PGHS-2 action and the downstream effect of HPA axis stimulation are stimulated by NMDA-mediated glutamatergic neurotransmission. Chronically catheterized late-gestation fetal sheep (n = 8) were injected with NMDA (1 mg iv). All responded with increases in fetal plasma ACTH and cortisol concentrations. Pretreatment with resveratrol (100 mg iv, n = 5), a specific inhibitor of PGHS-1, did not alter the magnitude of the HPA axis response to NMDA. Pretreatment with nimesulide (10 mg iv, n = 6), a specific inhibitor of PGHS-2, significantly reduced the HPA axis response to NMDA. To further explore this interaction, we injected NMDA in six chronically catheterized fetal sheep that were chronically infused with nimesulide (n = 6) at a rate of 1 mg/day into the lateral cerebral ventricle for 5–7 days. In this group, there was no significant ACTH response to NMDA. Finally, we tested whether the HPA axis response to prostaglandin E2 (PGE2) is mediated by NMDA receptors. Seven chronically catheterized late-gestation fetal sheep were injected with 100 ng of PGE2, which significantly increased fetal plasma ACTH and cortisol concentrations. Pretreatment with ketamine (10 mg iv), an NMDA antagonist, did not alter the ACTH or cortisol response to PGE2. We conclude that generation of prostanoids via the action of PGHS-2 in the fetal brain augments the fetal HPA axis response to NMDA-mediated glutamatergic stimulation.
机译：胎儿大脑中产生的前列腺素是控制胎儿下丘脑-垂体-肾上腺（HPA）轴的机制的组成部分。该实验室先前的研究表明，前列腺素G / H合酶同工酶2（PGHS-2）抑制作用可降低胎儿HPA轴对脑灌注不足的反应，阻止胎儿血浆ACTH浓度升高，并延迟分娩。我们还发现，N-甲基-d-天冬氨酸（NMDA）受体的阻滞降低了胎儿ACTH对脑灌注不足的反应。本研究旨在测试以下假设：NMDA介导的谷氨酸能神经传递刺激了PGHS-2的作用和HPA轴刺激的下游作用。长期插管的晚期妊娠胎羊（n = 8）被注射NMDA（1 mg iv）。所有人的反应均与胎儿血浆ACTH和皮质醇浓度增加有关。用白藜芦醇（100 mg iv，n = 5）（PGHS-1的特异性抑制剂）进行预处理不会改变HPA轴对NMDA的反应幅度。尼美舒利（10 mg iv，n = 6）（一种PGHS-2的特异性抑制剂）进行的预处理显着降低了HPA轴对NMDA的反应。为了进一步探讨这种相互作用，我们向六只经慢性导管插入的胎羊注射了NMDA，这些羊经尼美舒利（n = 6）的慢性注射以1 mg / day的速率注入脑侧脑室5-7天。在该组中，对NMDA没有明显的ACTH反应。最后，我们测试了NMDA受体是否介导了HPA轴对前列腺素E2（PGE2）的反应。向七只经慢性导管插管的晚期妊娠绵羊羊注射了100 ng PGE2，这显着增加了胎儿血浆ACTH和皮质醇的浓度。用氯胺酮（10 mg iv）（一种NMDA拮抗剂）进行预处理不会改变ACTH或皮质醇对PGE2的反应。我们得出结论，在胎儿大脑中通过PGHS-2的作用产生类前列腺素会增加胎儿HPA轴对NMDA介导的谷氨酸能刺激的反应。

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