Aldrich M S, Hollingsworth Z, Penney J B
Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.
Neurology. 1992 Feb;42(2):410-5. doi: 10.1212/wnl.42.2.410.
Although the pathology of human narcolepsy is unknown, studies of human and canine narcolepsy have suggested that dopamine metabolism may be disturbed. We used quantitative autoradiography to assess dopamine D1- and D2-receptor binding in basal ganglia and amygdala of five narcoleptic and 17 control human brains. In caudate, narcoleptic brains had a statistically significant increase of 57% in D1-receptor binding, and large but not significant increases of 54% in medial globus pallidus D1 binding, 63% in caudate D2-receptor binding, 95% in lateral globus pallidus D2 binding, and 93% in lateral amygdala D2 binding. We found no major changes in the putamen or in the basal or accessory basal nuclei of the amygdala. These results suggest that narcolepsy is associated with upregulation of dopamine receptors in specific areas of the brain, although medications used prior to death may have contributed to the findings.
尽管人类发作性睡病的病理机制尚不清楚，但对人类和犬类发作性睡病的研究表明，多巴胺代谢可能受到干扰。我们使用定量放射自显影术评估了5例发作性睡病患者和17例对照者人脑基底神经节和杏仁核中多巴胺D1和D2受体的结合情况。在尾状核中，发作性睡病患者的大脑D1受体结合率在统计学上显著增加了57%，苍白球内侧D1结合增加了54%、尾状核D2受体结合增加了63%、苍白球外侧D2结合增加了95%、杏仁核外侧D2结合增加了93%，虽增加幅度大但无统计学意义。我们发现壳核以及杏仁核的基底核或副基底核没有重大变化。这些结果表明，发作性睡病与大脑特定区域多巴胺受体的上调有关，尽管死亡前使用的药物可能对这些发现有一定影响。
