Inhibition of hormonally induced inositol trisphosphate production in Transfected GH4</ sup>C1 cells: A novel role for the D5 subtype of the dopamine receptor.
Inhibition of hormonally induced inositol trisphosphate production in Transfected GH4</ sup>C1 cells: A novel role for the D5 subtype of the dopamine receptor.
复制标题
转染的 GH4C1 细胞中激素诱导的三磷酸肌醇产生的抑制：多巴胺受体 D5 亚型的新作用。
DOI：
10.1159/000054421
复制
发表时间：
1999
影响因子：
4.1
通讯作者：
Sidhu,A
中科院分区：
文献类型：
--
作者：
White,BH;Kimura,K;Sidhu,A
We have previously found that the D [sub 5] dopamine receptor couples to a G-protein other than G [sub s] α, and could be involved in signaling pathways other than regulation of adenylyl cyclase. To describe interactions of the D [sub 5] receptor with cellular effectors, we used GH [sub 4] C [sub 1] cells transfected with cDNA for the human D [sub 5] receptor. Thyrotropin-releasing hormone (TRH, 100 nM) stimulated accumulation of inositol phosphates (IPs) fivefold in D [sub 5] GH [sub 4] C [sub 1] cells. Dopamine (DA, 10 μM) inhibited TRH-stimulated IP values by 29%; at higher concentrations (100 μM), maximal inhibition of 61% was observed. The D [sub 5] agonist SKF R-38393 (10 μM) mimicked this effect (28% inhibition). SCH 23390, a D [sub 5] antagonist, blocked the inhibition caused by both DA and SKF R-38393. Spiperone, a D [sub 2] receptor antagonist, did not block the inhibition. The D [sub 2] agonist (±)-2-(N-phenylethyl-N-propyl) amino-5-hydroxytetralin (PPHT) did not inhibit TRH-stimulated IP production, nor did it augment the effect of D [sub 5] agonists. The DA-mediated suppression of IP levels was not sensitive to pertussis toxin; cholera toxin blocked both TRH stimulation and DA suppression of IP accumulation in response to 100 nM TRH. Neither dibutyryl cAMP nor forskolin lowered IP formation in response to TRH. Phorbol ester decreased TRH-stimulated IP accumulation in D [sub 5] GH [sub 4] C [sub 1] cells; however, an inhibitor of protein kinase C (PKC) did not block the effect of DA.
