Chavoix C, Samson Y, Pappata S, Prenant C, Mazière M, Seck A, Agid Y
Département de Biologie, Hôpital d'Orsay, France.
Can J Neurol Sci. 1990 Nov;17(4):404-9. doi: 10.1017/s0317167100030973.
Central type benzodiazepine receptors were studied in 9 patients with Friedreich's ataxia and 12 healthy subjects using positron emission tomography (PET) and [11C]Ro 15-1788, a specific antagonist of the central type benzodiazepine receptors, as radioligand. A standard PET procedure was used in 5 patients and 8 controls to obtain brain kinetics of the total binding of the radioligand. The remaining subjects were intravenously injected with a saturating dose of unlabeled Ro 15-1788, 30 minutes after the tracer injection, to determine the nondisplaceable binding of [11C]Ro 15-1788. A semi-quantitative method was used to quantify the [11C]Ro 15-1788 data. None of the quantification indices in the cerebellar hemispheres, or in the other brain areas investigated, was significantly modified in patients with Friedreich's ataxia. These findings suggest that brain benzodiazepine receptors are unaffected in Friedreich's ataxia.
使用正电子发射断层扫描（PET）和作为放射性配体的中枢型苯二氮䓬受体特异性拮抗剂[11C]Ro 15-1788，对9例弗里德赖希共济失调患者和12名健康受试者的中枢型苯二氮䓬受体进行了研究。5例患者和8名对照采用标准PET程序，以获得放射性配体总结合的脑动力学数据。其余受试者在注射示踪剂30分钟后静脉注射饱和剂量的未标记Ro 15-1788，以确定[11C]Ro 15-1788的不可置换结合。采用半定量方法对[11C]Ro 15-1788数据进行定量分析。弗里德赖希共济失调患者小脑半球或其他所研究脑区的定量指标均无显著改变。这些发现表明，弗里德赖希共济失调患者脑内苯二氮䓬受体未受影响。
