Activation of central D-1 dopamine receptors stimulates oxytocin release in the lactating rat: evidence for involvement of the hypothalamic paraventricular and supraoptic nuclei.
Activation of central D-1 dopamine receptors stimulates oxytocin release in the lactating rat: evidence for involvement of the hypothalamic paraventricular and supraoptic nuclei.
复制标题
中枢 D-1 多巴胺受体的激活刺激哺乳大鼠催产素释放：下丘脑室旁核和视上核参与的证据。
DOI：
10.1159/000126253
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发表时间：
1992
影响因子：
4.1
通讯作者：
Crowley,WR
中科院分区：
文献类型：
--
作者：
Parker,SL;Crowley,WR
多巴胺（DA）刺激泌乳大鼠催产素（OT）释放的作用是通过D-1受体亚型实现的。由于尚未确定介导这种效应的神经位点，本研究的目的是测试在将D-1 DA受体激动剂中枢施用到第三脑室（3V）或直接施用到头侧室旁核/前连合核区（PVN/ACN）、中央室旁核区或视上核（SON）后，泌乳大鼠中的OT释放是否会升高，它们都含有OT神经分泌细胞。将不锈钢套管直接植入哺乳期大鼠的上述区域之一，或植入内侧基底下丘脑（MBH）的腹内侧区，或PVN/ACN或SON背侧的部位，作为解剖学对照。恢复6-7天后，每只动物接受心房内插管进行连续采血，并在24小时后用于实验。将动物与其窝仔分开，并在基础血液采样一段时间后，接受媒介物、D-1 DA受体激动剂SKF-38393或D-2 DA受体激动剂喹吡罗的中心微量注射，并定期取出血液样品60 min。在每个部位注射血管紧张素II（Ang II，100 ng）作为OT释放的阳性对照。向3V注射SKF-38393（12.5或50 µg/5 µl）导致血浆OT浓度呈统计学显著性和剂量依赖性增加，经静脉给予特异性D-1 DA受体拮抗剂SCH-23390（1.2 mg/kg）预处理后，该增加减弱。向SON区域单侧注射SKF-38393（8 µg）也导致血浆OT浓度显著增加，而向PVN部位注射该药物后，血浆OT浓度增加幅度较小。用D-1 DA拮抗剂全身预处理也阻断了SKF-38393在SON中的作用。在MBH或背部对照部位给予SKF-38393后，或在任何中枢注射溶媒或D-2激动剂喹吡罗后，血浆OT浓度均未发生显著变化。Ang Ⅱ对3V、PVN、SON和MBH的OT释放有明显的刺激作用，而对PVN和SON背侧的对照部位则无明显的刺激作用。目前的研究结果扩展了以前的观察，D-1 DA受体介导的中枢多巴胺能刺激OT分泌的哺乳大鼠，并建议SON区域可能是一个重要的位点，这种效果。
The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls. After 6-7 days of recovery, each animal received an intra-atrial cannula for sequential blood sampling, and was used in experiments 24 h later. Animals were separated from their litters, and following a period of basal blood sampling, received central microinjections of either vehicle, the D-1 DA receptor agonist SKF-38393, or the D-2 DA receptor agonist quinpirole, and blood samples were removed periodically for 60 min. An injection of angiotensin II (Ang II, 100 ng) was made into each site as a positive control for OT release. Injection of SKF-38393 (12.5 or 50 µg/5 µl) into the 3V resulted in a statistically significant and dose-releated increase in plasma OT concentrations, which was attenuated by intravenous pretreatment with the specific D-1 DA receptor antagonist, SCH-23390 (1.2 mg/kg). Unilateral injection of SKF-38393 (8 µg) into the SON region also produced a significant increase in plasma OT concentrations, while more modest increases followed injection of this agent into the PVN sites. Systemic pretreatment with the D-1 DA antagonist also blocked the effect of SKF-38393 in the SON. Plasma OT concentrations were not significantly changed after administration of SKF-38393 into the MBH or to dorsal control sites, or after any central injections of vehicle or the D-2 agonist quinpirole. Ang II markedly stimulated OT release after administration to 3V, PVN, SON and MBH, but not to the control sites dorsal to the PVN and SON. The present findings extend previous observations that D-1 DA receptors mediate the central dopaminergic stimulation of OT secretion in the lactating rat, and suggest that the SON region may be an important locus for this effect.