Knable M B, Hyde T M, Egan M F, Tosayali M, Wyatt R J, Kleinman J E
Clinical Brain Disorders Branch, National Institute of Mental Health, St. Elizabeths Hospital, Washington, DC 20032.
Brain Res. 1994 May 23;646(2):217-22. doi: 10.1016/0006-8993(94)90081-7.
Rats treated with haloperidol that developed vacuous chewing movements (VCM), a possible animal model of tardive dyskinesia, were studied with quantitative autoradiography for dopamine type-1 (D1) and type-2 (D2) receptors as well as dopamine re-uptake sites. Haloperidol increased striatal D2 receptors, but did not affect D1 receptors or the dopamine re-uptake site. D2 receptor increases occurred in rats with and without VCMs. In so far as VCM is a model for tardive dyskinesia, haloperidol induced increases in striatal D2 receptors do not appear to be etiologic for these abnormal movements.
用氟哌啶醇治疗后出现空嚼运动（VCM）的大鼠，VCM是迟发性运动障碍的一种可能动物模型，采用定量放射自显影术研究其多巴胺1型（D1）和2型（D2）受体以及多巴胺再摄取位点。氟哌啶醇增加了纹状体D2受体，但不影响D1受体或多巴胺再摄取位点。D2受体增加发生在有和没有VCM的大鼠中。就VCM是迟发性运动障碍的模型而言，氟哌啶醇诱导的纹状体D2受体增加似乎不是这些异常运动的病因。
