Prolactin prevents acute stress-induced hypocalcemia and ulcerogenesis by acting in the brain of rat
Prolactin prevents acute stress-induced hypocalcemia and ulcerogenesis by acting in the brain of rat
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DOI：
10.1210/en.2003-1446
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发表时间：
2004-04-01
期刊：
影响因子：
4.8
通讯作者：
Nakashima, K
中科院分区：
文献类型：
--
作者：
Fujikawa, T;Soya, H;Nakashima, K
应激可导致大鼠低钙血症和溃疡形成。在应激状态下，大鼠循环中的催乳素(PRL)迅速而短暂地升高，这种增强的PRL诱导了大鼠脑脉络丛中的PRL受体(PRLR)。在本研究中，我们利用水中的束缚应激来阐明大鼠脑内PRLR介导PRL对应激性低钙血症和溃疡形成的保护作用的机制。我们发现大鼠PRL是通过下丘脑中的长形PRLR起作用的。随之而来的是大脑脉络丛中PRLR长形mRNA表达的增加，这对水引起的低钙血症和胃侵蚀时的束缚应激具有保护作用。我们还发现PRL诱导室旁核PRLR蛋白和促肾上腺皮质激素释放因子mRNA的表达。这些结果表明，PRL水平在应激反应中升高，它从循环进入脑脊液，作用于中枢神经系统，从而在帮助保护急性应激性低钙血症和胃侵蚀方面发挥重要作用。
Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. Wealso show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.