IN-SITU HYBRIDIZATION ANALYSIS OF VASOPRESSIN GENE-TRANSCRIPTION IN THE PARAVENTRICULAR AND SUPRAOPTIC NUCLEI OF THE RAT - REGULATION BY STRESS AND GLUCOCORTICOIDS
IN-SITU HYBRIDIZATION ANALYSIS OF VASOPRESSIN GENE-TRANSCRIPTION IN THE PARAVENTRICULAR AND SUPRAOPTIC NUCLEI OF THE RAT - REGULATION BY STRESS AND GLUCOCORTICOIDS
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DOI：
10.1002/cne.903630103
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发表时间：
1995-12-04
影响因子：
2.5
通讯作者：
HERMAN, JP
中科院分区：
文献类型：
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作者：
HERMAN, JP
下丘脑含有精氨酸加压素的神经元是调节下丘脑-垂体-肾上腺皮质应激反应的中枢回路的主要元件。众所周知，加压素的释放和合成是由压力刺激引起的。本研究旨在评估应激对下丘脑室旁核 (PVN) 和视上核 (SON) 特定加压素神经元群中加压素转录和 mRNA 表达的影响。内含子和外显子定向原位杂交分析用于检查加压素异核 (hn) 基因转录和 mRNA 水平的应激调节。使用皮下植入递送恒定生理剂量皮质酮的肾上腺切除的大鼠来测试糖皮质激素对加压素诱导的作用。将颗粒植入肾上腺切除的大鼠体内，在缺乏糖皮质激素应激反应能力的情况下，可以保持正常的垂体-肾上腺张力。早在应激开始后 30 分钟，正常大鼠和肾上腺切除皮质酮替代大鼠中就观察到内侧小细胞 PVN 中加压素异核 (hn) RNA 的升高。在对照大鼠中，加压素 hnRNA 水平在 120 分钟后恢复到基线。相比之下，在肾上腺切除的皮质酮替代大鼠中，加压素 hnRNA 在抑制后 120 分钟仍保持升高，表明糖皮质激素应激反应可快速抑制加压素转录。在约束诱导后 90 分钟，在对照大鼠的小细胞 PVN 中观察到应激后加压素 mRNA 水平的显着变化，并在 120 分钟时恢复到正常表达谱。肾上腺切除替换的大鼠在所有检查时间点均显示加压素 mRNA 表达升高。在任何时间点都没有观察到大细胞加压素的细胞核发生变化，这表明大细胞加压素不是由这种特定的应激范式诱导的。因此，在小细胞室旁核神经元中，加压素基因被应激迅速诱导。抑制诱导的加压素转录上调受到糖皮质激素分泌的限制，这与糖皮质激素负反馈对细胞小神经元中加压素基因的直接作用一致。 (C) 1995 Wiley-Liss, Inc.
Hypothalamic arginine vasopressin-containing neurons are prime elements in central circuits regulating the hypothalamo-pituitary-adrenocortical stress response. It is known that release and synthesis of vasopressin are cued by stressful stimuli. The present study was designed to assess effects of stress on vasopressin transcription and mRNA expression in defined populations of vasopressin neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. Intron- and exon-directed in situ hybridization analyses were used to examine stress regulation of vasopressin heteronuclear (hn) gene transcription and mRNA levels. Actions of glucocorticoids on vasopressin induction were tested using adrenalectomized rats implanted with subcutaneous pellets delivering a constant, physiological dose of corticosterone. Pellet implantation into adrenalectomized rats allows for normal pituitary-adrenal tone in the absence of the ability to mount glucocorticoid stress responses. Elevation of vasopressin heteronuclear (hn) RNA in the medial parvicellular PVN was observed in both normal and adrenalectomized-corticosterone replaced rats as early as 30 minutes after stress initiation. In control rats, vasopressin hnRNA levels returned to baseline by 120 minutes. In contrast, vasopressin hnRNA remained elevated 120 minutes post-restraint in adrenalectomized-corticosterone replaced rats, indicating that the glucocorticoid stress response acts to rapidly inhibit vasopressin transcription. Significant changes in post-stress vasopressin mRNA levels were observed in the parvicellular PVN of control rats 90 minutes following restraint induction, returning to normal expression profiles by 120 minutes. Adrenalectomized-replaced rats showed elevated vasopressin mRNA expression at all time points examined. No changes were observed in magnocellular vasopressin-containing nuclei at any time point, suggesting that magnocellular vasopressin is not induced by this particular stress paradigm. Thus, in parvicellular paraventricular nucleus neurons the vasopressin gene is rapidly induced by stress. Restraint-induced up-regulation of vasopressin transcription is limited by glucocorticoid secretion, consistent with direct actions of glucocorticoid negative feedback on the vasopressin gene in parvicellular neurons. (C) 1995 Wiley-Liss, Inc.