Regulation of CART mRNA in the rat nucleus accumbens via D3 dopamine receptors
Regulation of CART mRNA in the rat nucleus accumbens via D3 dopamine receptors
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DOI：
10.1016/j.neuropharm.2005.12.007
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发表时间：
2006-06-01
影响因子：
4.7
通讯作者：
Kuhar, Michael J.
中科院分区：
文献类型：
--
作者：
Hunter, Richard G.;Jones, Douglas;Kuhar, Michael J.
多种研究表明，伏隔核内的CART(NAcc)参与了精神刺激剂的作用。为了更详细地了解多巴胺是否以及如何参与NAcc中CART mRNA的调节，本研究对单个受体进行了研究。给成年雄性大鼠单独和联合应用D1激动剂二氢呋喃西定和D1拮抗剂SCH23,390，但原位杂交未见CART基因表达的变化。D2/3激动剂奎比罗单独给药或与D2选择性拮抗剂L741,626或D3选择性拮抗剂GR103,691联合给药。昆匹罗使CART基因的mRNA减少了43%。这种作用可被D3拮抗剂GR103,691阻断，但不能被D2拮抗剂L741,626阻断。急性奎比罗后CART多肽水平也显示出类似的下降。D3突变小鼠NAcc中的CART mRNA水平高于野生型动物，但用喹比罗处理突变体后，CART表达没有像野生型啮齿动物那样下降。这些发现表明，CART受NAcc中的多巴胺调节，至少部分受D3多巴胺受体的调节。(C)2005爱思唯尔有限公司。保留所有权利。
A variety of studies indicate that CART in the nucleus accumbens (NAcc) is involved in the action of psychostimulants. In order to understand in more detail if and how dopamine is involved in the regulation of CART mRNA in the NAcc, the present studies of individual receptors were performed. The D1 agonist, dihydrexidine, and the D1 antagonist, SCH23,390, were administered separately and in combination to adult male rats; however, no changes were found in CART mRNA as measured by in situ hybridization. The D2/3 agonist, quinpirole, was administered either separately or in combination with the D2 selective antagonist, L741,626, or the D3 selective antagonist, GR103,691. Quinpirole produced a decrease in CART mRNA of up to 43%. This effect was blocked by pretreatment with the D3 antagonist GR103, 691, but not by the D2 antagonist, L741,626. CART peptide levels showed a similar decrement after acute quinpirole. CART mRNA levels in the NAcc of D3 mutant mice were found to be higher than that in wild-type animals, but treating the mutants with quinpirole failed to produce a decrease in CART expression like that observed in wild-type rodents. These findings demonstrate that CART is regulated by dopamine in the NAcc, at least partly by D3 dopamine receptors. (c) 2005 Elsevier Ltd. All rights reserved.