Fujikawa Takahiko, Soya Hideaki, Tamashiro Kellie L K, Sakai Randall R, McEwen Bruce S, Nakai Naoya, Ogata Masato, Suzuki Ikukatsu, Nakashima Kunio
Department of Biochemistry, Faculty of Medicine, Mie University, Japan.
Endocrinology. 2004 Apr;145(4):2006-13. doi: 10.1210/en.2003-1446. Epub 2004 Jan 8.
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. We also 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.
应激会导致大鼠出现低钙血症和溃疡形成。在处于应激状态的大鼠中，可观察到循环催乳素（PRL）迅速且短暂地增加，并且这种升高的PRL会诱导大鼠脑脉络丛中的PRL受体（PRLR）。在本研究中，我们采用水浸束缚应激来阐明大鼠脑中的PRLR介导PRL对抗应激诱导的低钙血症和溃疡形成的保护作用的机制。我们发现大鼠PRL通过下丘脑的长型PRLR发挥作用。随后，脑脉络丛中长型PRLR mRNA表达增加，这为对抗水浸束缚应激诱导的低钙血症和胃糜烂提供了保护。我们还发现PRL可诱导室旁核中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，应激会使PRL水平升高，它从循环进入脑脊液作用于中枢神经系统，从而在帮助抵御急性应激诱导的低钙血症和胃糜烂方面发挥重要作用。
