Liu Nu-yun, Zhang Lin, Wang Xiao-ning, Zhang Lu
Institute of Molecular Immunology, Southern Medical University, Guangzhou 510515, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2006 Jun;26(6):715-8.
To study the role of dopamine receptors in the regulation of the activity of transcription factor cAMP response element-binding protein (CREB) after cocaine treatment.
By using dopamine receptor antagonists SCH23390 and nafadotride, the activation of CREB by D1 and D3 dopamine receptors after cocaine treatment and role of extracellular signal-regulated kinase (ERK) in cocaine-induced CREB activation were examined by Western blotting, which was also employed for determination of the effect of SCH23390 and nafadotride on CREB activation.
D1 receptor antagonist could inhibit cocaine-induced CREB activation, while D3 receptor antagonist enhanced cocaine-induced CREB activation. Dopamine receptor antagonists SCH23390 and nafadotride did not induce CREB activation. SL327, a MEK inhibitor, inhibited cocaine-induced CREB activation.
D1 and D3 dopamine receptors can oppositely regulate CREB activation after cocaine treatment and this regulation depends on ERK signaling pathway.
研究多巴胺受体在可卡因处理后对转录因子环磷腺苷反应元件结合蛋白（CREB）活性调节中的作用。
使用多巴胺受体拮抗剂SCH23390和萘法唑酮，通过蛋白质免疫印迹法检测可卡因处理后D1和D3多巴胺受体对CREB的激活作用以及细胞外信号调节激酶（ERK）在可卡因诱导的CREB激活中的作用，该方法也用于测定SCH23390和萘法唑酮对CREB激活的影响。
D1受体拮抗剂可抑制可卡因诱导的CREB激活，而D3受体拮抗剂增强可卡因诱导的CREB激活。多巴胺受体拮抗剂SCH23390和萘法唑酮未诱导CREB激活。MEK抑制剂SL327抑制可卡因诱导的CREB激活。
可卡因处理后，D1和D3多巴胺受体可对CREB激活产生相反调节作用，且这种调节依赖于ERK信号通路。
