Kulak Jennifer M, Musachio John L, McIntosh J Michael, Quik Maryka
The Parkinson's Institute, 1170 Morse Avenue, Sunnyvale, CA 94089-1605, USA.
J Pharmacol Exp Ther. 2002 Nov;303(2):633-9. doi: 10.1124/jpet.102.039347.
In the present study we used the nicotinic ligand 5-iodo-A-85380 [5-iodo-3(2(S)-azetidinylmethoxy)pyridine], which selectively binds to beta2-containing nicotinic acetylcholine receptors, to elucidate the nicotinic receptor subtypes affected by nigrostriatal damage in the monkey. Autoradiographic studies in control monkeys showed that 5-[(125)I]A-85380 ([(125)I]A-85380) binds throughout the brain with the characteristics of a nicotinic receptor ligand. Competition experiments with cytisine and nicotine yielded K(i) values of approximately 1 and 10 nM, respectively, with complete inhibition of [(125)I]A-85380 binding at a 10(-6) M concentration of these ligands. In contrast, alpha-conotoxin MII blocked radioligand binding in the striatum by 30% at the highest concentrations, suggesting that a subset of striatal [(125)I]A-85380 sites are alpha-conotoxin MII-sensitive. Monkeys treated with the nigrostriatal neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine showed a selective decrease in striatal [(125)I]A-85380 sites, with a 42% reduction in the caudate and putamen of animals with moderate nigrostriatal lesioning and a 53% decline in the striatum of severely lesioned animals. Our previous work had demonstrated that there were two populations of nicotinic receptors eliminated after nigrostriatal damage, an alpha-conotoxin MII-sensitive and an alpha-conotoxin MII- resistant subtype. Analysis of both striatal [(125)I]A-85380 and [(125)I]epibatidine competition studies extend our earlier studies by demonstrating that the alpha-conotoxin MII-sensitive sites eliminated after moderate nigrostriatal lesioning appear to be composed of two nicotinic receptor subtypes. The data may be important for potential therapeutic approaches because they suggest that there are at least three populations of nicotinic receptors in monkey striatum, of which two are selectively vulnerable to nigrostriatal damage, while the third is more resistant.
在本研究中,我们使用了烟碱样配体5-碘-A-85380 [5-碘-3(2(S)-氮杂环丁烷甲氧基)吡啶],它能选择性地与含β2的烟碱型乙酰胆碱受体结合,以阐明受猴子黑质纹状体损伤影响的烟碱型受体亚型。对对照猴子的放射自显影研究表明,5-[(125)I]A-85380([(125)I]A-85380)以烟碱型受体配体的特征在全脑结合。与金雀花碱和尼古丁的竞争实验分别得出K(i)值约为1 nM和10 nM,在这些配体浓度为10(-6) M时完全抑制[(125)I]A-85380的结合。相比之下,α-芋螺毒素MII在最高浓度时使纹状体中的放射性配体结合减少30%,这表明纹状体中一部分[(125)I]A-85380位点对α-芋螺毒素MII敏感。用黑质纹状体神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶处理的猴子,纹状体中[(125)I]A-85380位点出现选择性减少,中度黑质纹状体损伤动物的尾状核和壳核减少42%,重度损伤动物的纹状体减少53%。我们之前的工作已经证明,黑质纹状体损伤后有两类烟碱型受体被消除,一类是对α-芋螺毒素MII敏感的亚型,另一类是对α-芋螺毒素MII耐药的亚型。对纹状体[(125)I]A-85380和[(125)I]爱必妥定竞争研究的分析扩展了我们早期的研究,表明中度黑质纹状体损伤后被消除的对α-芋螺毒素MII敏感的位点似乎由两种烟碱型受体亚型组成。这些数据对于潜在的治疗方法可能很重要,因为它们表明猴子纹状体中至少有三类烟碱型受体,其中两类对黑质纹状体损伤选择性敏感,而第三类更具抗性。