Volkow N D, Fowler J S, Wang G J, Hitzemann R, Logan J, Schlyer D J, Dewey S L, Wolf A P
Medical Department, Brookhaven National Laboratory, Upton, New York 11973.
Synapse. 1993 Jun;14(2):169-77. doi: 10.1002/syn.890140210.
Decreased dopaminergic function has been postulated to underlie cocaine addiction. To examine the possibility that dysfunction of brain regions subserved by the dopamine system could promote cocaine self-administration, positron emission tomography and a dual-tracer approach was used to examine dopamine D2 receptor availability and regional brain glucose metabolism in cocaine abusers. When compared to normal controls, cocaine abusers showed significant decreases in dopamine D2 receptor availability which persisted 3-4 months after detoxification. Decreases in dopamine D2 receptor availability were associated with decreased metabolism in several regions of the frontal lobes, most markedly orbito-frontal cortex and cingulate gyri. Dopamine dysregulation of these brain areas which are involved in the channeling of drive and affect could lead to loss of control resulting in compulsive drug-taking behavior.
多巴胺能功能降低被认为是可卡因成瘾的基础。为了研究多巴胺系统所支配的脑区功能障碍是否会促进可卡因自我给药,采用正电子发射断层扫描和双示踪剂方法检测可卡因滥用者的多巴胺D2受体可用性和脑区葡萄糖代谢。与正常对照组相比,可卡因滥用者的多巴胺D2受体可用性显著降低,且在戒毒后3 - 4个月仍持续存在。多巴胺D2受体可用性降低与额叶多个区域的代谢降低有关,最明显的是眶额皮质和扣带回。这些参与驱力和情感传导的脑区多巴胺调节异常可能导致失控,从而产生强迫性吸毒行为。