[125I]CGP 42112揭示了1-甲基-4-苯基吡啶（MPP+）诱导的脑损伤中的一种非血管紧张素II结合位点。
[125I]CGP 42112 reveals a non-angiotensin II binding site in 1-methyl-4-phenylpyridine (MPP+)-induced brain injury.
作者信息
Viswanathan M, de Oliveira A M, Wu R M, Chiueh C C, Saavedra J M
机构信息
Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.
出版信息
Cell Mol Neurobiol. 1994 Feb;14(1):99-104. doi: 10.1007/BF02088592.
Abstract
- Intracerebral injection of the oxidative metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridine (MPP+), into the substantia nigra of adult rats resulted in a lesion at the injection site. 2. Using autoradiography, we localized specific [125I]CGP 42112 binding that was not recognized by angiotensin II or angiotensin II AT1 or AT2 receptor-selective ligands. 3. Our results suggest that [125I]CGP 42112 may be binding to activated microglia that appear at the lesion site.
摘要
- 向成年大鼠黑质内注射1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）的氧化代谢产物1-甲基-4-苯基吡啶（MPP+），在注射部位造成了损伤。2. 利用放射自显影技术，我们定位了特异性的[125I]CGP 42112结合，该结合不被血管紧张素II或血管紧张素II AT1或AT2受体选择性配体识别。3. 我们的结果表明，[125I]CGP 42112可能与出现在损伤部位的活化小胶质细胞结合。
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