Endogenous opioid peptides contribute to suckling-induced prolactin release by suppressing tyrosine hydroxylase activity and messenger ribonucleic acid levels in tuberoinfundibular dopaminergic neurons
Endogenous opioid peptides contribute to suckling-induced prolactin release by suppressing tyrosine hydroxylase activity and messenger ribonucleic acid levels in tuberoinfundibular dopaminergic neurons
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DOI：
10.1210/en.139.6.2857
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发表时间：
1998-06-01
期刊：
影响因子：
4.8
通讯作者：
Voogt, JL
中科院分区：
文献类型：
--
作者：
Arbogast, LA;Voogt, JL
内源性阿片肽参与控制哺乳期乳汁中催乳素的升高。这项研究考察了内源性阿片肽在哺乳期抑制漏斗状多巴胺能神经元活动中的作用。在第一个实验中，哺乳期的大鼠经常接触幼崽。静脉滴注阿片受体拮抗剂纳洛酮(NAL，60 mg/kg.h)或生理盐水12h，每隔2 h采血。在输液开始后的4、6、8和12小时，NAL将循环PRL水平抑制到控制值的36%以下。在NAL注射结束时，测定柄-正中隆起的酪氨酸羟化酶(TH)活性和弓状核TH信使RNA的信号水平。注射NAL 12h后，TH活性和TH信使RNA信号水平分别增加2.5倍和2.7倍。尽管两组幼崽在一起的时间相似，但NAL处理组的幼崽在12h的NAL输注期间体重没有增加，而对照组(8只幼崽)体重增加了5g。在第二个实验中，幼崽在12h的NAL输注前被从水坝中移走，11h后被送回。在输注之前，幼崽分离期间每隔3小时采集一次血，与幼崽团聚后每隔15分钟采集一次血液。在分离期间，对照组和NAL处理组大鼠的血浆PRL浓度在1~15 ng/ml之间变化不大。NAL处理大鼠的哺乳诱导的PRL激增明显减弱到对照水平(350-650 ng/ml)的9-25%。在哺乳1h后，NAL处理组大鼠的柄-正中隆起的TH活性是对照组的4.5倍。在1小时哺乳期间，接受NAL处理的大鼠的窝重增长明显较少。这些数据表明，内源性阿片肽是增加哺乳反应中PRL释放的不可或缺的组成部分，它们在哺乳期通过抑制TH基因的表达部分地降低了结节漏斗多巴胺能神经元的活性。
The endogenous opioid peptides have been implicated in the control of the suckling-induced PRL rise during lactation. This study examined the role of the endogenous opioid peptides in suppressing tuberoinfundibular dopaminergic neuronal activity during lactation. In the first experiment, lactating rats were constantly exposed to pups. Naloxone (NAL; 60 mg/kg.h; iv), an opioid receptor antagonist, or saline was infused for 12 h. Blood was collected before and at 2-h intervals during the infusion. NAL suppressed circulating PRL levels to less than 36% of control values at 4, 6, 8, and 12 h after the onset of the infusion. Tyrosine hydroxylase (TH) activity in the stalk-median eminence and TH messenger RNA signal levels in the arcuate nucleus were determined at the end of the NAL infusion. TH activity and TH messenger RNA signal levels were increased 2.5- and 2.7-fold, respectively, after the 12-h NAL infusion. Even though the time spent with their pups was similar between the two groups, the pups in the NAL-treated group failed to gain weight during the 12-h NAL infusion period, whereas the control litters (8 pups) gained 5 g. In a second experiment, pups were removed from the dams before the 12-h NAL infusion and were returned after 11 h. Blood was collected before the infusion, at 3-h intervals during the pup separation period, and at 15-min intervals after reunion with the pups. Plasma PRL in control and NAL-treated rats was law (1-15 ng/ml) and similar during the separation period. The suckling-induced PRL surge in NAL-treated rats was markedly attenuated to 9-25% of control levels (350-650 ng/ml). After a 1-h suckling episode, TH activity in the stalk-median eminence of NAL-treated rats was 4.5-fold greater than controls. Litter weight gains were significantly less in NAL-treated rats during the 1-h suckling episode. These data indicate that the endogenous opioid peptides are an integral component for increasing PRL release in response to suckling and they act to decrease tuberoinfundibular dopaminergic neuronal activity during lactation, in part, by suppressing TH gene expression.