The neuronal NOS inhibitor L-MIN, but not 7-NINA, reduces neurotoxic effects of chronic intrastriatal administration of quinolinic acid

被引:9
作者
Bazzett, T
Geiger, A
Coppola, B
Albin, R
机构
[1] SUNY Geneseo, Dept Psychol, Geneseo, NY 14454 USA
[2] Univ Michigan, Dept Neurol, Ann Arbor, MI 48104 USA
[3] Univ Michigan, Dept Chem, Ann Arbor, MI 48104 USA
[4] Ann Arbor VAMC, Ctr Geriatr Res Educ & Clin, Ann Arbor, MI 48104 USA
关键词
NMDA receptor; Huntington's disease; excitotoxicity; neuroprotection; basal ganglia; hydroxyl radical; nitric oxide; indazole;
D O I
10.1016/S0006-8993(97)00962-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Rat striata were exposed to 15 mM quinolinic acid (QUIN), or QUIN plus the nitric oxide synthase inhibitors S-methyl-L-thiocitrulline dihydrochloride (L-MIN) or 7-nitroindazole monosodium salt (7-NINA) for 21 days. Co-administration of 100 mu M or 1 mM L-MIN with QUIN significantly reduced lesion volume compared to QUIN alone. Co-administration of 1 mu M or 10 mu M L-MIN with QUIN had no significant effect. There was no significant effect of 7-NINA co-administered with QUIN compared to QUIN alone. L-MIN reduction of lesion volume supports the contention that neuronal nitric oxide synthase is a mediator of excitotoxic injury. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:229 / 232
页数:4
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