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Expression of striatal adenosine and dopamine receptors in mice deficient in the p50 subunit of NF-kappa B

机译：NF-κBp50亚基缺失的小鼠纹状体腺苷和多巴胺受体的表达

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The striatal dopamine D2 receptor (D2R) and adenosine A2A receptor (A2AAR) exhibit mutually antagonistic effects through physical interactions and by differential modulation of post-receptor signaling pathways. The expression of the A2AAR and the D2R is differentially regulated by nuclear factor-kappa B (NF-kappa B). In this report, we determined the role of NF-kappa B in regulation of these receptors by comparing mice deficient in the NF-kappa B p50 subunit (p50 KO) with genetically intact B6129PF2/J (F2) mice. Quantification of adenosine receptor (AR) subtypes in mouse striatum by real time PCR, immunocytochemistry and radioligand binding assays showed more A2AAR but less A I AR in p50 KO mice as compared with F2 mice. Striata from p50 KO mice also had less D2R mRNA and [H-3]-methylspiperone binding than did striata from F2 mice. G(alpha olf) and G(alpha s) proteins, which are transducers of A2AAR signals, were also present at a higher level in striata from the p50 KO versus F2 mice. In contrast, the G(alpha i1) protein, which transduces signals from the AIAR and D2R, was significantly reduced in striata from p50 KO mice. Behaviorally, p50 KO mice exhibited increased locomotor activity relative to that of F2 mice after caffeine ingestion. These data are consistent with a role for the NF-kappa B in the regulation of A1AR, A2AAR, D2R and possibly their coupling G proteins in the striatum. Dysregulation of these receptors in the striata of p50 KO mice might sensitize these animals to locomotor stimulatory action of caffeine. (C) 2007 Elsevier Inc. All rights reserved.
机译：纹状体多巴胺D2受体（D2R）和腺苷A2A受体（A2AAR）通过物理相互作用和受体后信号传导途径的差异调节，表现出相互拮抗的作用。 A2AAR和D2R的表达受核因子-κB（NF-κB）的差异调节。在本报告中，我们通过比较缺乏NF-κBp50亚基（p50 KO）的小鼠和基因上完整的B6129PF2 / J（F2）小鼠，确定了NF-κB在调节这些受体中的作用。通过实时PCR，免疫细胞化学和放射性配体结合测定对小鼠纹状体中腺苷受体（AR）亚型的定量显示，与F2小鼠相比，p50 KO小鼠中的A2AAR较多，而AIIA较少。与来自F2小鼠的纹状体相比，来自p50 KO小鼠的纹状体还具有较少的D2R mRNA和[H-3]-甲基哌啶酮结合。 G（alpha olf）和G（alpha s）蛋白是A2AAR信号的转导者，它们在p50 KO小鼠和F2小鼠的纹状体中也以较高水平存在。相反，转导来自AIAR和D2R的信号的G（alpha i1）蛋白在来自p50 KO小鼠的纹状体中显着减少。从行为上讲，摄入咖啡因后，p50 KO小鼠相对于F2小鼠表现出增加的运动活性。这些数据与NF-κB在调节A1AR，A2AAR，D2R以及可能在纹状体中偶联G蛋白的作用一致。这些受体在p50 KO小鼠的纹状体中的失调可能使这些动物对咖啡因的运动刺激作用敏感。 （C）2007 Elsevier Inc.保留所有权利。

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