ADENOSINE A(2) RECEPTORS STIMULATE C-FOS EXPRESSION IN STRIATAL NEURONS OF 6-HYDROXYDOPAMINE-LESIONED RATS
ADENOSINE A(2) RECEPTORS STIMULATE C-FOS EXPRESSION IN STRIATAL NEURONS OF 6-HYDROXYDOPAMINE-LESIONED RATS
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DOI：
10.1016/0306-4522(94)00602-2
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发表时间：
1995-07-01
期刊：
影响因子：
3.3
通讯作者：
DICHIARA, G
中科院分区：
文献类型：
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作者：
MORELLI, M;PINNA, A;DICHIARA, G
在正常大鼠或多巴胺能黑质纹状体神经元单侧B-羟基多巴胺损伤的大鼠中，研究了腺苷A（2a）受体激动剂CGS 21680给药后早期基因c-fos的诱导。CGS 21680（2.5 mg/kg）诱导6-羟基多巴胺损伤的纹状体中的c-Sos表达，而高达40 mg/kg不能诱导完整纹状体或正常大鼠纹状体中的c-fos。东莨菪碱（5 mg/kg）阻断毒蕈碱受体可部分阻止CGS 21680诱导的6-羟基多巴胺损伤纹状体中c-fos表达，而喹吡罗（0.5 mg/kg）刺激多巴胺D-2受体可完全逆转CGS 21680诱导的6-羟基多巴胺损伤纹状体中c-fos表达。反过来，CGS 21680部分逆转c-fos的表达诱导quinpirole在病变苍白球。CGS 21680，此外，剂量依赖性地减少喹吡罗诱导的转向行为结果表明，CGS 21680通过直接和间接机制诱导纹状体c-fos表达，其机制与A（2a）受体刺激cAMP形成或乙酰胆碱释放的能力有关，从而激活c-fos。fos通过毒蕈碱受体。
The induction of the early-gene c-fos after administration of the adenosine A(2a) receptor agonist CGS 21680, was studied in the striatum of normal rats or in rats with a unilateral B-hydroxydopamine lesion of the dopaminergic nigrostriatal neurons. CGS 21680 (2.5 mg/kg) induces c-Sos expression in the 6-hydroxydopamine-lesioned striatum, while up to 40 mg/kg fails to induce c-fos in the intact striatum or in the striatum of normal rats. Blockade of muscarinic receptors by scopolamine (5 mg/kg) partially prevents, and stimulation of dopamine D-2 receptors by quinpirole (0.5 mg/kg) completely reverses, CGS 21680-induced c-fos expression in the 6-hydroxydopamine-lesioned striatum. In turn, CGS 21680 partially reverses c-fos expression induced by quinpirole in the lesioned globus pallidus. CGS 21680, in addition, dose-dependently reduces the turning behavior induced by quinpirole (0.5 mg/kg) in 6-hydroxydopamine-lesioned rats.The results suggest that CGS 21680 induces c-fos expression in the striatum through direct and indirect mechanisms related to the ability of A(2a) receptors to stimulate cyclic AMP formation or acetylcholine release which in turn would activate c-fos through muscarinic receptors.