Vallone D, Pellecchia M T, Morelli M, Verde P, DiChiara G, Barone P
International Institute of Genetics and Biophysics, Napoli, Italy.
Brain Res Mol Brain Res. 1997 Dec 15;52(2):307-17. doi: 10.1016/s0169-328x(97)00253-2.
Rats with unilateral dopamine denervation exhibit turning behaviour in response to the selective D1 agonist SKF 38393 only after a previous exposure to dopamine agonists. We demonstrate here that this 'priming' phenomenon is related to both an increased expression of the pre-existing AP-1 complex and the occurrence of novel AP-1 complexes which are formed by FosB- and JunD-related proteins. While the former protein is expressed as a consequence of the dopamine denervation, the latter is related to the first exposure to a dopamine agonist. Pre-treatment with MK-801, an antagonist for glutamatergic receptors, prevents both the priming development and the AP-1 compositional changes. Rotational behaviour induced by SKF 38393 closely correlates with the presence of the priming AP-1 complexes, regardless of the capability of the D1 agonist to induce the immediate-early gene cFos.
单侧多巴胺去神经支配的大鼠仅在先前接触多巴胺激动剂后，才会对选择性D1激动剂SKF 38393表现出旋转行为。我们在此证明，这种“启动”现象与预先存在的AP-1复合物表达增加以及由FosB和JunD相关蛋白形成的新型AP-1复合物的出现有关。虽然前一种蛋白是多巴胺去神经支配的结果，但后一种蛋白与首次接触多巴胺激动剂有关。用谷氨酸能受体拮抗剂MK-801预处理可防止启动的发展和AP-1组成的变化。SKF 38393诱导的旋转行为与启动AP-1复合物的存在密切相关，而与D1激动剂诱导即早基因cFos的能力无关。
