GT1b ganglioside induces death of dopaminergic neurons in rat mesencephalic cultures

被引:19
作者
Chung, ES
Joe, EH
Ryu, JK
Kim, J
Lee, YB
Cho, KG
Oh, YJ
Maeng, SH
Baik, HH
Kim, SU
Jin, BK [1 ]
机构
[1] Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 442749, South Korea
[2] Ajou Univ, Sch Med, Dept Pharmacol, Suwon 442749, South Korea
[3] Ajou Univ, Sch Med, Dept Neurosurg, Suwon 442749, South Korea
[4] Yonsei Univ, Coll Sci, Dept Biol, Seoul 120749, South Korea
[5] Seoul Natl Univ, Coll Med, Dept Pharmacol, Seoul 110799, South Korea
[6] Kyung Hee Univ, Coll Med, Dept Biochem, Seoul 130701, South Korea
关键词
dopaminergic neurons; microglia; nitric oxide (NO); tissue culture; trisialoganglioside (GT1b); Tyrosine hydroxylase (TH);
D O I
10.1097/00001756-200103050-00036
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We examined neurotoxicity of GT1b against dopaminergic neurons in vitro. Cultures of mesencephalic cells deprived of serum underwent the loss of 19% of tyrosine hydroxylase immunopositive (TH-ip) neurons. In cultures deprived of serum. treatment with 10-30 mug/ml GT1b attenuated the number of TH-ip neurons by 26-69%, respectively. compared to non-treated cultures. Intriguingly, cultures deprived of serum were more vulnerable to GT1b-induced neurotoxicity. Application of 60 mug/ml GT1b to cultures grown in serum containing media resulted in the loss of 26% of TH-ip neurons, similar to that (28%) observed in serum-deprived cultures treated with 10 mug/ml GT1b. Moreover, in our cultures, absence of nitric oxide (NO) production after GT1b treatment was obvious. The present results strongly suggest direct neurotoxic actions of GT1b against dopaminergic neurons regardless of NO. NeuroReport 12:611-614 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:611 / 614
页数:4
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