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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Nitric oxide stimulates ACTH secretion and the transcription of the genes encoding for NGFI-B, corticotropin-releasing factor, corticotropin-releasing factor receptor type 1, and vasopressin in the hypothalamus of the intact rat.
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Nitric oxide stimulates ACTH secretion and the transcription of the genes encoding for NGFI-B, corticotropin-releasing factor, corticotropin-releasing factor receptor type 1, and vasopressin in the hypothalamus of the intact rat.

机译：一氧化氮刺激完整大鼠下丘脑中NGFI-B，促肾上腺皮质激素释放因子，促肾上腺皮质激素释放因子受体1型和加压素的编码基因的转录和转录。

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摘要

We investigated the effect of the intracerebroventricular injection of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal response of hypothalamic neurons responsible for this release. Rats that were administered SIN-1 showed significant elevations in plasma ACTH levels, a response that was virtually abolished by antibodies against corticotropin-releasing factor (CRF) and significantly blunted by vasopressin (VP) antiserum. SIN-1 also upregulated heteronuclear (hn) transcripts for CRF and VP and messenger RNA (mRNA) levels for the immediate early gene NGFI-B and for CRF receptor type 1 (CRF-R(1)) in the parvocellular portion of the paraventricular nucleus (PVN) of the hypothalamus. Blockade of prostaglandin synthesis with ibuprofen did not alter the ACTH or the PVN response to SIN-1. The central nucleus of the amygdala and the supraoptic nucleus, regions that are involved in autonomic adjustments to altered cardiovascular activity, also responded to SIN-1 with elevated NGFI-B mRNA levels. However, the only change in mean arterial blood pressure caused by this NO donor was a transient and modest increase. To our knowledge, this is the first demonstration that in the intact rat NO stimulates the activity of PVN neurons that control the hypothalamic-pituitary-adrenal axis. It must be noted, however, that our results do not allow us to determine whether this effect was direct or mediated through PVN afferents. This study should help resolve the controversy generated by the use of isolated brain tissues to investigate the net effect of NO on hypothalamic peptide production.
机译：我们调查了脑室内注射一氧化氮（NO）供体3-吗啉代-亚砜亚胺（SIN-1）对肾上腺皮质激素（ACTH）释放和下丘脑神经元负责该释放的神经元反应的影响。给予SIN-1的大鼠血浆ACTH水平显着升高，这种反应实际上被抗促肾上腺皮质激素释放因子（CRF）的抗体所消除，而被抗血管加压素（VP）的抗血清明显减弱。 SIN-1还上调了室旁小细胞部分的立即早期基因NGFI-B和1型CRF受体（CRF-R（1））的CRF和VP和信使RNA（mRNA）水平的异核（hn）转录本。下丘脑核（PVN）。用布洛芬阻断前列腺素合成不会改变ACTH或PVN对SIN-1的反应。杏仁核的中央核和视上核（参与自主调节心血管活动的区域）也对SIN-1产生了NGFI-B mRNA升高的反应。然而，由该NO供体引起的平均动脉血压的唯一变化是短暂而适度的升高。据我们所知，这是在完整大鼠中NO刺激控制下丘脑-垂体-肾上腺轴的PVN神经元活性的第一个证明。但是必须注意，我们的结果不允许我们确定这种效果是直接的还是通过PVN传入介导的。这项研究应有助于解决因使用分离的脑组织调查NO对下丘脑肽产生的净作用而引起的争议。

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