D2 Dopamine receptor subtype mediates the inhibitory effect of dopamine on TRH-induced prolactin release from the bullfrog pituitary
D2 Dopamine receptor subtype mediates the inhibitory effect of dopamine on TRH-induced prolactin release from the bullfrog pituitary
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DOI：
10.1016/j.ygcen.2010.05.008
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发表时间：
2010-09-01
影响因子：
2.7
通讯作者：
Kobayashi, Tetsuya
中科院分区：
文献类型：
--
作者：
Nakano, Masaki;Minagawa, Atsuko;Kobayashi, Tetsuya
已知哺乳动物中的多巴胺受体由两种D1样受体（D1和D5）和三种D2样受体（D2、D3和D4）组成。本研究的目的是确定多巴胺受体亚型介导的抑制作用的多巴胺对催乳素（PRL）的释放从两栖动物垂体。牛蛙（Rana catesbeiana）的远侧叶灌流，并通过同源酶免疫测定法测定流出介质中释放的PRL的量。TRH可刺激垂体分泌PRL。多巴胺抑制TRH诱导的PRL释放升高。Quinpirole（一种D2受体激动剂）也抑制TRH对PRL释放的刺激作用，而SKF-38393（一种D1受体激动剂）没有这种作用。多巴胺对TRH诱导的垂体PRL释放的抑制作用可通过向培养基中加入L-741，626（一种选择性D2受体拮抗剂）而无效，但不能通过加入SCH-23390（一种选择性D1受体拮抗剂）而无效。这些数据表明，多巴胺对TRH诱发的牛蛙脑垂体PRL释放的抑制作用是通过D2多巴胺受体介导的。(C)2010年爱思唯尔公司All rights reserved.
Dopamine receptors in mammals are known to consist of two D1-like receptors (D1 and D5) and three D2-like receptors (D2, D3 and D4). The aim of this study was to determine the dopamine receptor subtype that mediates the inhibitory action of dopamine on the release of prolactin (PRL) from the amphibian pituitary. Distal lobes of the bullfrog (Rana catesbeiana) were perifused and the amount of PRL released in the effluent medium was measured by means of a homologous enzyme-immunoassay. TRH stimulated the release of PRL from perifused pituitaries. Dopamine suppressed TRH-induced elevation of PRL release. Quinpirole (a D2 receptor agonist) also suppressed the stimulatory effect of TRH on the release of PRL, whereas SKF-38393 (a D1 receptor agonist) exhibited no such an effect. The inhibitory action of dopamine on TRH-induced PRL release from the pituitary was nullified by the addition of L-741,626 (a selective D2 receptor antagonist) to the medium, but not by the addition of SCH-23390 (a selective D1 receptor antagonist). These data indicate that the inhibitory effect of dopamine on TRH-evoked PRL release from the bullfrog pituitary gland is mediated through D2 dopamine receptors. (C) 2010 Elsevier Inc. All rights reserved.