Ruskin D N, Marshall J F
Department of Psychobiology, University of California, Irvine, CA 92717, USA.
Brain Res. 1995 Dec 12;703(1-2):156-64. doi: 10.1016/0006-8993(95)01093-9.
Studies of the globus pallidus (GP) and subthalamic nucleus (STN) have emphasized the role of D2 dopamine receptors, although effects of D1 receptor activation on GP firing rate and STN metabolism have been reported, especially in rats with nigrostriatal lesions. This study systematically investigated the effects of D1 and D2 receptor activation on the activity of the GP and STN in intact and 6-OHDA-lesioned rats using immunostaining for the immediate-early gene Fos. In intact rats, the D1 agonist SKF 38393 (20.0 mg/kg) produced a five-fold potentiation of the GP Fos expression due to the D2 agonist quinpirole produced significant Fos expression. In rats with prior nigrostriatal lesions, SKF 38393 (4.0 or 20.0 mg/kg) increased Fos immunostaining in both the GP and STN, while quinpirole increased it only in the GP. SKF 38393 effects in the GP and STN of nigrostriatal-lesioned rats were blocked completely by SCH 23390, and unaffected by eticlopride. These results are a novel demonstration of control of Fos expression by dopaminergic drugs in the STN and by D1 agonists in the GP.
对苍白球(GP)和丘脑底核(STN)的研究一直强调D2多巴胺受体的作用,尽管已有报道称D1受体激活对GP放电率和STN代谢有影响,尤其是在黑质纹状体损伤的大鼠中。本研究使用即刻早期基因Fos免疫染色,系统地研究了D1和D2受体激活对完整大鼠和6-羟基多巴胺(6-OHDA)损伤大鼠的GP和STN活性的影响。在完整大鼠中,D1激动剂SKF 38393(20.0mg/kg)使GP Fos表达增强了五倍,而D2激动剂喹吡罗产生了显著的Fos表达。在先前有黑质纹状体损伤的大鼠中,SKF 38393(4.0或20.0mg/kg)增加了GP和STN中的Fos免疫染色,而喹吡罗仅增加了GP中的Fos免疫染色。黑质纹状体损伤大鼠的GP和STN中SKF 38393的作用被SCH 23390完全阻断,且不受依替必利的影响。这些结果首次证明了多巴胺能药物对STN中Fos表达的控制以及D1激动剂对GP中Fos表达的控制。