Xu Jian-Fen, Chen Xue-Qun, Du Ji-Zeng
Division of Neurobiology and Physiology, College of Life Sciences, Zhejiang University, Yuquan Campus, Hangzhou 310027, PR China.
Horm Behav. 2006 Feb;49(2):181-9. doi: 10.1016/j.yhbeh.2005.06.004. Epub 2005 Aug 15.
We have reported that, in rats, hypoxia (10.8% O2) stimulates prolactin (PRL) release from the pituitary. This study is designed to compare the response of pituitary PRL to acute hypoxia (AH), continual hypoxia (CH), intermittent hypoxia (IH), cold, and restraint, individually and combined with hypoxia. This study also investigates the involvement of the corticotropin-releasing hormone receptor 1 (CRH R1) in the hypoxia-induced PRL response. Hypoxia was induced by exposing the rats to high altitudes of 2 km (16.0% O2) or 5 km (10.8% O2). The PRL levels in the pituitary (iPRL) and in plasma (pPRL) were measured by immunocytochemistry and RIA assay, respectively. The acute hypoxia of 5 km for 2-24 h caused a biphasic change (early decrease and late increase) of PRL. Both CH and IH at 2 or 5 km for 1-5 days markedly increased pPRL but decreased iPRL. Continual severe hypoxia (10.8% O2) for periods of 10, 15, and 25 days significantly enhanced pPRL but this effect was less marked at the lower altitude (16.0% O2) and did not occur during intermittent hypoxia (at both altitudes). The increased pPRL was significantly enhanced by restraint, restraint + hypoxia, hypoxia, and cold + hypoxia exposure. Treatment with a CRH R1 antagonist (CP-154,526) reversed hypoxia-decreased immunoreactive PRL and upregulated PRLmRNA in the pituitary. The data suggest that both CH and IH can stimulate rat PRL release in a time-course- and intensity-dependent manner. However, compared to the relatively low CH-induced response, restraint induced a more powerful response than either cold or hypoxia alone. CRH R1 mediates PRL secretion and PRL mRNA expression in the pituitary under hypoxic exposure. Hypoxia-enhanced PRL response over the lifespan may play a significant role in adaptation to an extreme environment.
我们曾报道，在大鼠中，低氧（10.8%氧气）会刺激垂体释放催乳素（PRL）。本研究旨在比较垂体PRL对急性低氧（AH）、持续低氧（CH）、间歇性低氧（IH）、寒冷和束缚的反应，以及这些因素单独或与低氧联合作用时的反应。本研究还调查了促肾上腺皮质激素释放激素受体1（CRH R1）在低氧诱导的PRL反应中的作用。通过将大鼠暴露于2千米（16.0%氧气）或5千米（10.8%氧气）的高海拔环境来诱导低氧。分别通过免疫细胞化学和放射免疫分析测定垂体（iPRL）和血浆（pPRL）中的PRL水平。5千米的急性低氧持续2 - 24小时会导致PRL出现双相变化（早期下降和后期上升）。2千米或5千米的CH和IH持续1 - 5天均显著增加pPRL，但降低iPRL。持续严重低氧（10.8%氧气）10、15和25天会显著提高pPRL，但在较低海拔（16.0%氧气）时这种作用不太明显，并且在间歇性低氧（在两个海拔高度）期间未出现。束缚、束缚 + 低氧、低氧以及寒冷 + 低氧暴露会显著增强升高的pPRL。用CRH R1拮抗剂（CP - 154,526）处理可逆转低氧降低的免疫反应性PRL，并上调垂体中的PRLmRNA。数据表明，CH和IH均可在时间进程和强度依赖的方式下刺激大鼠PRL释放。然而，与相对较低的CH诱导反应相比，束缚诱导的反应比单独的寒冷或低氧更强烈。CRH R1在低氧暴露下介导垂体中PRL的分泌和PRL mRNA的表达。低氧增强的PRL反应在整个生命周期中可能在适应极端环境中发挥重要作用。
