Nagy G M, Arendt A, Bánky Z, Halász B
Second Department of Anatomy, Semmelweis Medical University, Budapest, Hungary.
Endocrinology. 1992 Feb;130(2):819-24. doi: 10.1210/endo.130.2.1733729.
The tuberoinfundibular dopaminergic neurons projecting to the median eminence are well accepted as a major physiological regulator of adenohypophyseal PRL secretion. However, recent evidence has shown that dopamine (DA) in the neurointermediate lobe also has an inhibitory effect on PRL secretion by anterior pituitary. Since the neurointermediate is innervated by the tuberohypophyseal dopaminergic (THDA) neurons, which is known to be selectively activated by dehydration of the animal, the aim of this study was to investigate the physiological role of the THDA system in PRL release during lactation. On the day of the experiments, the litters were separated from the mothers for 4 h before initiation of the suckling stimulus. The suckling-induced PRL surge was detected on three consecutive days. On the first day the normal response was tested; then immediately after taking the last blood samples, drinking solutions were changed to the high salt (2.5% saline) containing bottles or were taken away. Suckling-induced PRL response was significantly decreased after 24 h and almost completely blocked 48 h later in dehydrated mothers. This effect could be prevented by haloperidol (a DA receptor antagonist) pretreatment (0.1 mg/kg BW sc), and it was only transient because rehydration of the mothers reestablished basal as well as suckling-induced PRL response. In addition, the effect of an acute osmotic stimulus on the plasma PRL levels (injecting 0.5 ml 10% saline solution iv) was also tested. There was a marked and immediate decrease in PRL concentration within 15 min of injection. Domperidone, another DA receptor blocker (20 micrograms/rat iv) completely abolished the depletion of plasma PRL in response to 10% saline injection. These results support our assumption that the dopaminergic regulation of PRL secretion during lactation involves the THDA system. Furthermore, these data underline the importance of an interaction between regulation of PRL secretion and water and sodium homeostasis.
投射至正中隆起的结节漏斗多巴胺能神经元被公认为腺垂体催乳素（PRL）分泌的主要生理调节因子。然而，最近有证据表明，神经中间叶中的多巴胺（DA）对垂体前叶PRL的分泌也具有抑制作用。由于神经中间叶受结节垂体多巴胺能（THDA）神经元支配，已知该神经元会因动物脱水而被选择性激活，因此本研究的目的是探讨THDA系统在哺乳期PRL释放过程中的生理作用。在实验当天，幼崽在开始哺乳刺激前4小时与母亲分开。连续三天检测哺乳诱导的PRL激增。第一天测试正常反应；然后在采集最后一批血样后，立即将饮用溶液换成含高盐（2.5%盐水）的瓶子或拿走。脱水母亲在24小时后，哺乳诱导的PRL反应显著降低，48小时后几乎完全被阻断。这种效应可通过氟哌啶醇（一种DA受体拮抗剂）预处理（0.1mg/kg体重，皮下注射）来预防，并且只是短暂的，因为母亲补液后可恢复基础以及哺乳诱导的PRL反应。此外，还测试了急性渗透刺激对血浆PRL水平的影响（静脉注射0.5ml 10%盐水溶液）。注射后15分钟内PRL浓度显著且立即下降。多潘立酮，另一种DA受体阻滞剂（20微克/大鼠，静脉注射）完全消除了注射10%盐水后血浆PRL的减少。这些结果支持了我们的假设，即哺乳期PRL分泌的多巴胺能调节涉及THDA系统。此外，这些数据强调了PRL分泌调节与水和钠稳态之间相互作用的重要性。
