HYPOXIA-INDUCED NEUROTRANSMITTER DEFICITS IN NEONATAL RATS ARE PARTIALLY CORRECTED BY EXOGENOUS GM1 GANGLIOSIDE

被引：21
作者：
HADJICONSTANTINOU, M
YATES, AJ
NEFF, NH
机构：
[1] OHIO STATE UNIV, COLL MED,DEPT PHARMACOL,5198 GRAVES HALL, 333 W 10TH AVE, COLUMBUS, OH 43210 USA
[2] OHIO STATE UNIV, COLL MED, DEPT PSYCHIAT, COLUMBUS, OH 43210 USA
[3] OHIO STATE UNIV, COLL MED, DEPT PATHOL, COLUMBUS, OH 43210 USA
来源：
JOURNAL OF NEUROCHEMISTRY | 1990年 / 55卷 / 03期
关键词：
Biogenic amine‐containing neurons; Choline uptake; Dopamine uptake; Frontal cortex; GMI ganglioside; Hippocampus; Hypoxia; Neonatal rats; Neurodegeneration; Striatum;
D O I：
10.1111/j.1471-4159.1990.tb04571.x
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Abstract: Exposure of 7‐day‐old rats to 7% oxygen/balance nitrogen for 2 h results in selective changes of cholinergic, serotonergic, and dopaminergic neuronal markers in the frontal cortex, hippocampus, and striatum when evaluated 3 weeks after the insult. There is also about a 15% deficiency in brain weight. Treatment with GM1 ganglioside, 50 mg/ kg i.p., for 2 days before and for 3 weeks after the hypoxic insult partially corrects the neurodevelopmental abnormalities including the deficiency in brain weight. We conclude that GMI ganglioside might have therapeutic potential for treating suspected neonatal hypoxia. Copyright © 1990, Wiley Blackwell. All rights reserved
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页码：864 / 869
页数：6
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