INTRACELLULAR AND EXTRACELLULAR CHANGES OF AMINO-ACIDS IN THE CEREBRAL-CORTEX OF THE NEONATAL RAT DURING HYPOXIC-ISCHEMIA

被引:108
作者
ANDINE, P
SANDBERG, M
BAGENHOLM, R
LEHMANN, A
HAGBERG, H
机构
[1] GOTHENBURG UNIV,INST NEUROBIOL,POB 33031,S-40033 GOTHENBURG,SWEDEN
[2] GOTHENBURG UNIV,DEPT OBSTET & GYNECOL,S-41124 GOTHENBURG,SWEDEN
来源
DEVELOPMENTAL BRAIN RESEARCH | 1991年 / 64卷 / 1-2期
关键词
HYPOXIA; ISCHEMIA; AMINO ACID; GLYCINE; ENERGY METABOLITE; EXCITATORY AMINO ACID;
D O I
10.1016/0165-3806(91)90214-4
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Excitatory amino acids (EAAs) have been implicated to play a part in the development of hypoxic-ischemic brain injury in the neonate. The aim of the present study was to follow changes of intra- and extracellular (microdialysis) amino acids in the cerebral cortex in a model where cortical hypoxic-ischemic damage is produced consistently. Hypoxic-ischemia (unilateral ligation of the carotid artery + 2 h of exposure to 7.8% oxygen) caused a depletion of tissue ATP, phosphocreatine and glucose with a concomittant accumulation of AMP and lactic acid in cortical tissue. These changes were accompanied by a decrease of tissue aspartate and glutamine whereas the contents of gamma-aminobutyric acid GABA), phenylalanine, leucine, isoleucine, valine and alanine increased. In the extracellular fluid GABA, glutamate, aspartate, taurine, glycine and alanine all increased multi-fold during hypoxic-ischemia. Aspartate and glutamate returned to near initial levels 2 h after the end of the insult, whereas the elevation of glycine persisted during recovery. In conclusion, the high extracellular levels of EAAs and glycine may exert injurious effects during and after hypoxic-ischemia.
引用
收藏
页码:115 / 120
页数:6
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