Savasta M, Dubois A, Benavidès J, Scatton B
Laboratoires d'Etudes et de Recherches Synthélabo (L.E.R.S.), Biology Department, Bagneux, France.
Neurosci Lett. 1988 Feb 15;85(1):119-24. doi: 10.1016/0304-3940(88)90440-5.
The precise topographical changes in striatal D1 and D2 dopamine receptor density that occurred after chronic treatment with haloperidol or SCH 23390 or after 6-hydroxydopamine-induced lesion of the mesostriatal dopaminergic pathway have been studied autoradiographically in the rat. Repeated treatment with SCH 23390 (0.5 mg/kg i.p., 21 days) caused an almost similar increase in [3H]SCH 23390 binding sites in the different striatal subregions whereas lesion of the dopaminergic pathway was ineffective. Subacute administration of haloperidol (2 mg/kg i.p., 18 days) or lesion of dopaminergic afferents provoked an increase in [3H]spiperone binding which was restricted to the ventro- and dorsolateral striatal sectors.
利用放射自显影技术在大鼠身上研究了用氟哌啶醇或SCH 23390进行慢性治疗后，或在6-羟基多巴胺诱导的中脑纹状体多巴胺能通路损伤后，纹状体D1和D2多巴胺受体密度发生的精确地形学变化。重复给予SCH 23390（0.5mg/kg腹腔注射，共21天）导致不同纹状体亚区中[3H]SCH 23390结合位点出现几乎相似的增加，而多巴胺能通路损伤则无效。亚急性给予氟哌啶醇（2mg/kg腹腔注射，共18天）或多巴胺能传入神经损伤会引起[3H]螺哌隆结合增加，这一增加仅限于腹侧和背外侧纹状体区域。
