Plotsky P M, Neill J D
Endocrinology. 1982 Mar;110(3):691-6. doi: 10.1210/endo-110-3-691.
Previous in situ voltammetric microelectrode measurements of median eminence dopamine release during mammary nerve stimulation of anesthetized lactating rats revealed a transient (1-3 min) 70% decline of dopamine concentrations. This dopamine was believed to be destined for secretion into the hypophysial portal circulation, but direct experimental support for this supposition was lacking. Thus, in the present study, [3H]dopamine release into brief sequential samples of hypophysial portal blood was compared with dopamine release in the median eminence measured by voltammetry. Lactating female rats were urethane anesthetized, and the median eminence pituitary region was exposed. [3H]Tyrosine was injected into a jugular cannula (100 microCi) followed by continuous infusion (5 microCi/min). In a preliminary experiment, this regimen produced a steady state level of [3H]dopamine in the portal blood within 45 min. In subsequent experiments, portal blood was collected as sequential 3-min samples, and electrochemical sampling from a microelectrode placed in the median eminence occurred at 1-min intervals. Electrochemical current resulting from the oxidation of dopamine in the medial median eminence was unvarying throughout the 75-min experiment in control rats (n = 4) and during the 30-min control period preceding mammary nerve stimulation in the other group (n = 4). These results were parallel by [3H] dopamine levels in portal blood during the same periods of time. All animals showed simultaneous decreases in oxidation current and [3H]dopamine levels within 1-4 min after initiation of mammary nerve stimulation (respectively, 35 +/- 7% and 62.5 +/- 5.9%, mean +/- SEM). Significant increases in oxidation current, taking the form of brief 2- to 6-min pulses began within an average of 18.5 min after initiation of stimulation. Similar increases in [3H]dopamine levels in portal blood were also observed. These and earlier results demonstrate that mammary nerve stimulation (and by extension, suckling) induces a momentary, but profound, decrease in hypothalamic dopamine secretion which precedes or accompanies the rise in PRL secretion evoked by the same stimulus.
先前通过原位伏安微电极对麻醉的泌乳大鼠乳腺神经刺激期间正中隆起多巴胺释放的测量显示,多巴胺浓度出现短暂(1 - 3分钟)70%的下降。这种多巴胺被认为会分泌到垂体门脉循环中,但缺乏对这一假设的直接实验支持。因此,在本研究中,将[3H]多巴胺释放到垂体门脉血的连续简短样本中的情况与通过伏安法测量的正中隆起处多巴胺释放情况进行了比较。泌乳雌性大鼠用乌拉坦麻醉,暴露正中隆起垂体区域。将[3H]酪氨酸注入颈静脉插管(100微居里),随后持续输注(5微居里/分钟)。在一个初步实验中,该方案在45分钟内使门脉血中[3H]多巴胺达到稳态水平。在随后的实验中,以连续3分钟的样本收集门脉血,同时每隔1分钟从置于正中隆起的微电极进行电化学采样。在对照组大鼠(n = 4)的75分钟实验期间以及另一组(n = 4)乳腺神经刺激前30分钟的对照期内,正中隆起内侧多巴胺氧化产生的电化学电流保持不变。这些结果与同一时间段内门脉血中[3H]多巴胺水平平行。所有动物在乳腺神经刺激开始后1 - 4分钟内氧化电流和[3H]多巴胺水平同时下降(分别为35±7%和62.5±5.9%,平均值±标准误)。刺激开始后平均18.5分钟内,氧化电流以短暂的2至6分钟脉冲形式显著增加。门脉血中[3H]多巴胺水平也出现类似增加。这些以及早期结果表明,乳腺神经刺激(进而哺乳)会诱发下丘脑多巴胺分泌瞬间但显著的减少,这一减少先于或伴随同一刺激引起的催乳素分泌增加。