Moos F, Richard P
Brain Res. 1982 Jun 10;241(2):249-60. doi: 10.1016/0006-8993(82)91061-7.
The involvement of dopamine in the release of oxytocin and vasopressin was investigated in lactating rats during suckling or after changes in plasma osmolality. The effects of intraventricular injections of dopamine, agonists and antagonists, were tested on electrical unit activity of oxytocinergic or vasopressinergic cells in the paraventricular nucleus, on intramammary pressure (index of oxytocin release) and diuresis (index of vasopressin release). In urethane-anaesthetized lactating suckled rats, dopamine (1 microgram), apomorphine (2.5 and 5 micrograms) facilitated the established milk-ejection reflex, increasing the frequency and the amplitude of neurosecretory bursts of oxytocinergic cells. They also triggered the reflex in lactating rats without milk-ejections during suckling. The small doses injected were in no way such as to induce an acceleration in firing rate of oxytocinergic cells or an increase in mammary pressure. In alcohol-loaded rats, during water diuresis, dopamine (2 micrograms) and apomorphine (5 micrograms) activated the depressed vasopressinergic cells and inhibited diuresis. These facilitatory effects were progressive, reaching a maximum 10-15 min after injection. Haloperidol (5 micrograms) and alpha-flupentixol (10 micrograms) had an inhibitory effect on both types of neurosecretory cells in urethane-anaesthetized rats. They prevented the reflex activation of oxytocinergic cells induced by suckling and of vasopressinergic cells after a hyperosmotic stimulus (1 ml i.p 9% NaCl solution). These inhibitory effects were not of the "all-or-none' type. So, we can postulate that dopamine regulates the reflex release of oxytocin and vasopressin in the hypothalamus. On the one hand, dopamine permits and controls the periodic activation of oxytocinergic cells as long as the mothers are being suckled. On the other hand, it modulates the activity of vasopressinergic cells whenever the plasma osmolality changes.
研究了多巴胺在哺乳期大鼠哺乳期间或血浆渗透压改变后对催产素和血管加压素释放的影响。通过脑室内注射多巴胺、激动剂和拮抗剂，检测其对室旁核中催产素能或血管加压素能细胞的电单位活动、乳腺内压力（催产素释放指标）和利尿（血管加压素释放指标）的作用。在氨基甲酸乙酯麻醉的哺乳期哺乳大鼠中，多巴胺（1微克）、阿扑吗啡（2.5微克和5微克）促进已建立的喷乳反射，增加催产素能细胞神经分泌爆发的频率和幅度。它们还能触发哺乳期间无喷乳的哺乳期大鼠的反射。注射的小剂量药物绝不会引起催产素能细胞放电率加快或乳腺压力增加。在饮水利尿的酒精负荷大鼠中，多巴胺（2微克）和阿扑吗啡（5微克）激活受抑制的血管加压素能细胞并抑制利尿。这些促进作用是渐进性的，注射后10 - 15分钟达到最大值。氟哌啶醇（5微克）和α-氟哌噻吨（10微克）对氨基甲酸乙酯麻醉大鼠的两种神经分泌细胞均有抑制作用。它们可防止哺乳诱导的催产素能细胞反射激活以及高渗刺激（腹腔注射1毫升9%氯化钠溶液）后血管加压素能细胞的反射激活。这些抑制作用并非“全或无”类型。因此，我们可以推测多巴胺在下丘脑中调节催产素和血管加压素的反射性释放。一方面，只要母亲在哺乳，多巴胺就允许并控制催产素能细胞的周期性激活。另一方面，每当血浆渗透压发生变化时，它就调节血管加压素能细胞的活动。
