Kim H S, Park W K, Jang C G, Oh S
Department of Pharmacology, College of Pharmacy, Chungbuk National University, Cheongju, Korea.
Brain Res Bull. 1996;40(3):201-7. doi: 10.1016/0361-9230(96)00006-8.
Repeated administration of cocaine led to increases in ambulation-accelerating activity (sensitization) and conditioned place preference (CPP). Dopamine (DA)-receptor supersensitivity was also developed in cocaine-induced sensitized and CPP mice. An N-methyl-D-aspartate (NMDA)-receptor antagonist, MK-801, blocked simultaneously developments of cocaine-induced behavioral sensitization, CPP, and DA-receptor supersensitivity. Furthermore, MK-801 inhibited a apomorphine-induced striatal dopaminergic action: climbing behavior. These results suggest that the cocaine-induced dopaminergic behaviors such as sensitization to ambulatory activity and CPP may be produced via activation of the NMDA receptor. The development of postsynaptic DA-receptor supersensitivity may be an underlying common mechanism that mediates cocaine-induced behavioral sensitization and CPP.
重复给予可卡因会导致行走加速活动增加（敏化）和条件性位置偏爱（CPP）。在可卡因诱导的敏化和CPP小鼠中还出现了多巴胺（DA）受体超敏反应。N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801可同时阻断可卡因诱导的行为敏化、CPP和DA受体超敏反应的发展。此外，MK-801抑制阿扑吗啡诱导的纹状体多巴胺能作用：攀爬行为。这些结果表明，可卡因诱导的多巴胺能行为，如对行走活动的敏化和CPP，可能是通过NMDA受体的激活产生的。突触后DA受体超敏反应的发展可能是介导可卡因诱导的行为敏化和CPP的潜在共同机制。
