Rupniak N M, Tye S J, Iversen S D
Merck, Sharp and Dohme Research Laboratories, Neuroscience Research Centre, Harlow, Essex, UK.
J Neurol Sci. 1992 Jul;110(1-2):222-7. doi: 10.1016/0022-510x(92)90031-f.
Peripheral toxicity may explain the disappointing therapeutic effects of nonselective muscarinic agonists in Alzheimer's disease. Partial agonists might exhibit an improved therapeutic index. We compare the central and peripheral cholinergic effects of RS86 with the M1/M3 partial agonists AF 102B and L-689,660 ((-)-3-[2-6 chloropyrazin)yl]-1-azabicyclo[2.2.2]octane) in primates. Administration of RS86 (1.5-2.25 mg/kg i.m.) or L-689,660 (0.1-0.3 mg/kg i.m.), but not AF 102B (up to 6 mg/kg i.m.), caused partial reversal of the disruptive effects of scopolamine on cognition. However, performance remained significantly poorer than in untreated control animals. Adverse effects prevented examination of higher doses. Centrally-mediated hypothermia was induced by RS86 (0.05 mg/kg p.o.) and L-689,660 (0.01 mg/kg p.o.) but only by a high dose of AF 102B (7 mg/kg p.o.). The putative therapeutic advantages of partial M1/M3 agonists over RS86 are discussed.
外周毒性可能解释了非选择性毒蕈碱激动剂在阿尔茨海默病治疗中令人失望的疗效。部分激动剂可能具有更好的治疗指数。我们比较了RS86与M1/M3部分激动剂AF 102B和L-689,660((-)-3-[2-6氯吡嗪基]-1-氮杂双环[2.2.2]辛烷)在灵长类动物中的中枢和外周胆碱能效应。肌肉注射RS86(1.5 - 2.25毫克/千克)或L-689,660(0.1 - 0.3毫克/千克),而非AF 102B(高达6毫克/千克肌肉注射),可部分逆转东莨菪碱对认知的破坏作用。然而,其表现仍显著差于未治疗的对照动物。不良反应妨碍了更高剂量的检测。口服RS86(0.05毫克/千克)和L-689,660(0.01毫克/千克)可诱导中枢介导的体温过低,但仅高剂量的AF 102B(7毫克/千克口服)可诱导。文中讨论了M1/M3部分激动剂相对于RS86的假定治疗优势。