CHANGES IN EXTRACELLULAR AMINO-ACID NEUROTRANSMITTERS PRODUCED BY FOCAL CEREBRAL-ISCHEMIA

被引:155
作者
GRAHAM, SH
SHIRAISHI, K
PANTER, SS
SIMON, RP
FADEN, AI
机构
[1] UNIV CALIF SAN FRANCISCO,DEPT NEUROL,SAN FRANCISCO,CA 94143
[2] SAN FRANCISCO GEN HOSP,DEPT NEUROL,SAN FRANCISCO,CA 94110
关键词
Aspartate; Cerebral ischemia; GABA; Glutamate; Microdialysis;
D O I
10.1016/0304-3940(90)90799-F
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Excitatory amino acids (EAAs) have been implicated in the pathophysiology of cellular injury after brain ischemia. Changes in extracellular levels of amino acids in rat cerebral cortex after permanent proximal middle cerebral artery (MCA) occlusion were examined using microdialysis. Significant increases were found in dialysate concentrations of glutamate, aspartate and γ-aminobutyric acid (GABA) from the ischemic cortex during the first 90 min after MCA occlusion compared to pre-ischemic concentrations and contralateral hemispheric controls. Total tissue levels of these amino acids in the infarcted hemisphere 90 min after onset of ischemia were not different from the contralateral hemisphere. These results are consistent with the hypothesis that the release of EAAs may contribute to tissue damage in focal cerebral ischemia. © 1990.
引用
收藏
页码:124 / 130
页数:7
相关论文
共 26 条
[21]  
ROTHMAN S, 1984, J NEUROSCI, V4, P1884
[22]   GLUTAMATE AND THE PATHOPHYSIOLOGY OF HYPOXIC ISCHEMIC BRAIN-DAMAGE [J].
ROTHMAN, SM ;
OLNEY, JW .
ANNALS OF NEUROLOGY, 1986, 19 (02) :105-111
[23]  
SHIRAISHI K, IN PRESS J NEUROSCI
[24]   BLOCKADE OF N-METHYL-D-ASPARTATE RECEPTORS MAY PROTECT AGAINST ISCHEMIC DAMAGE IN THE BRAIN [J].
SIMON, RP ;
SWAN, JH ;
GRIFFITHS, T ;
MELDRUM, BS .
SCIENCE, 1984, 226 (4676) :850-852
[25]   ROLE FOR GAMMA-AMINOBUTYRIC ACID IN SELECTIVE VULNERABILITY IN GERBILS [J].
STERNAU, LL ;
LUST, WD ;
RICCI, AJ ;
RATCHESON, R .
STROKE, 1989, 20 (02) :281-287
[26]   HYPOGLYCEMIA-INDUCED NEURONAL DAMAGE PREVENTED BY AN N-METHYL-D-ASPARTATE ANTAGONIST [J].
WIELOCH, T .
SCIENCE, 1985, 230 (4726) :681-683