Crowley W R, Shyr S W, Kacsoh B, Grosvenor C E
Endocrinology. 1987 Jul;121(1):14-20. doi: 10.1210/endo-121-1-14.
The present experiments tested the involvement of central catecholaminergic systems in the suckling-induced release of oxytocin (OT) during lactation in the rat. In the first experiment, female rats in midlactation were separated from their offspring for 4 h and then allowed to suckle their litters for 30 or 60 min or to remain nonsuckled. The turnover rates of norepinephrine (NE) and dopamine (DA) were calculated from the rate of decline after synthesis inhibition. Suckling decreased the turnover rate of DA in the median eminence and in the neurointermediate lobe of the pituitary gland. Suckling increased the turnover rate of NE in the rostral paraventricular and supraoptic nuclei, areas that contain most of the OT cells that project to the neural lobe of the pituitary, and in the interstitial nucleus of the stria terminalis, but not in the arcuate or caudal paraventricular nuclei, median eminence, or neurointermediate lobe. In a second experiment, midlactating females received intracerebral microinjections of the catecholamine neurotoxin 6-hydroxydopamine or of vehicle into the vicinity of the paraventricular and supraoptic nuclei 1 week before a suckling test. The release of OT was completely prevented in 6-hydroxydopamine-treated animals, and NE was significantly decreased in the paraventricular, supraoptic, and arcuate nuclei. In a third study, the increase in plasma OT in response to suckling was prevented by stimulation of DA receptors with bromocriptine, while blockade of DA receptors with domperidone significantly increased plasma OT levels in nonsuckled lactating rats. These results suggest that suckling stimulation activates the noradrenergic innervation to the rostral paraventricular nucleus and to the supraoptic nucleus, which exerts an excitatory influence on the release of OT and decreases activity of the tuberohypophyseal DA system, which provides a tonic inhibitory influence over the secretion of OT.
本实验检测了中枢儿茶酚胺能系统在大鼠哺乳期吮乳诱导的催产素（OT）释放过程中的作用。在第一个实验中，将处于泌乳中期的雌性大鼠与其后代分离4小时，然后让它们给幼崽哺乳30或60分钟，或者不进行哺乳。去甲肾上腺素（NE）和多巴胺（DA）的周转率根据合成抑制后的下降速率计算得出。哺乳降低了正中隆起和垂体神经中间叶中DA的周转率。哺乳增加了室旁核前部和视上核中NE的周转率，这些区域包含大部分投射到垂体神经叶的OT细胞，以及终纹间质核中的NE周转率，但在弓状核或室旁核后部、正中隆起或神经中间叶中未增加。在第二个实验中，在哺乳测试前1周，给处于泌乳中期的雌性大鼠在室旁核和视上核附近脑室内微量注射儿茶酚胺神经毒素6-羟基多巴胺或溶剂。在接受6-羟基多巴胺处理的动物中，OT的释放被完全抑制，室旁核、视上核和弓状核中的NE显著减少。在第三个研究中，用溴隐亭刺激DA受体可阻止哺乳引起的血浆OT升高，而用多潘立酮阻断DA受体则显著提高未哺乳泌乳大鼠的血浆OT水平。这些结果表明，哺乳刺激激活了室旁核前部和视上核的去甲肾上腺素能神经支配，对OT的释放产生兴奋性影响，并降低了结节-垂体DA系统的活性，该系统对OT的分泌具有紧张性抑制作用。
