Little K Y, Gorebig J, Carroll F I, Mapili J, Meador-Woodruff J H
Department of Psychiatry, University of Michigan, Ann Arbor 48109, USA.
Brain Res. 1996 Dec 2;742(1-2):313-6. doi: 10.1016/s0006-8993(96)01033-5.
Depending on experimental conditions, chronic cocaine exposure can induce an increase in binding to the dopamine transporter (DAT). One possible mechanism for the cocaine-induced-upregulation in DAT binding sites is through stimulation of presynaptic D2 receptors by excess synaptic dopamine. To test this hypothesis, the present experiment examined in rats the effect of chronic quinpirole and apomorphine treatments on striatal DAT binding sites. Rats were chronically injected subcutaneously with either: quinpirole, 0.7 mg/kg body weight, apomorphine, 2.0 mg/kg body weight, or vehicle. Striatal DAT binding was then examined autoradiographically using the DAT-selective cocaine congeners [125I]RTI-121 and [3H]WIN 35428. Analysis of the results indicated that quinpirole and apomorphine administration did not alter DAT cocaine binding sites.
根据实验条件，长期接触可卡因可导致多巴胺转运体（DAT）结合增加。可卡因诱导DAT结合位点上调的一种可能机制是通过过量突触多巴胺刺激突触前D2受体。为了验证这一假设，本实验研究了大鼠长期使用喹吡罗和阿扑吗啡治疗对纹状体DAT结合位点的影响。大鼠被皮下长期注射以下药物之一：喹吡罗，0.7mg/kg体重；阿扑吗啡，2.0mg/kg体重；或溶剂。然后使用DAT选择性可卡因类似物[125I]RTI-121和[3H]WIN 35428通过放射自显影法检测纹状体DAT结合情况。结果分析表明，给予喹吡罗和阿扑吗啡不会改变DAT可卡因结合位点。
