HYPOXIC-ISCHEMIC DAMAGE IN THE NEONATAL BRAIN - EXCITATORY AMINO-ACIDS

被引:35
作者
HAGBERG, H [1 ]
机构
[1] GOTHENBURG UNIV,DEPT OBSTET & GYNECOL,S-41124 GOTHENBURG,SWEDEN
来源
DEVELOPMENTAL PHARMACOLOGY AND THERAPEUTICS | 1992年 / 18卷 / 3-4期
关键词
EXCITATORY AMINO ACIDS; NEONATAL; BRAIN; HYPOXIA; ISCHEMIA; BRAIN DAMAGE;
D O I
10.1159/000480613
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Perinatal brain damage is a major clinical problem. Recent studies suggest that excitatory amino acids (EAAs) may be important for the development of hypoxic-ischemic brain injury in the newborn. Experimental work demonstrates that the immature brain is hypersensitive to the toxic effects EAA ('excitotoxicity'), hypoxic-ischemia is accompanied by an extracellular overflow of EAAs and hypoxic-ischemic brain damage is reduced by EAA receptor antagonists. Clinical investigations demonstrate the presence of EAA receptors in vulnerable areas of the newborn human brain and the concentrations of EAAs in the cerebrospinal fluid are higher in asphyxiated than in control infants. Clincial studies are warranted to evaluate the importance of excitotoxicity for development of brain lesions after severe asphyxia.
引用
收藏
页码:139 / 144
页数:6
相关论文
共 53 条
  • [1] THE EXCITATORY AMINO-ACID ANTAGONIST KYNURENIC ACID ADMINISTERED AFTER HYPOXIC-ISCHEMIA IN NEONATAL RATS OFFERS NEUROPROTECTION
    ANDINE, P
    LEHMANN, A
    ELLREN, K
    WENNBERG, E
    KJELLMER, I
    NIELSEN, T
    HAGBERG, H
    [J]. NEUROSCIENCE LETTERS, 1988, 90 (1-2) : 208 - 212
  • [2] INTRACELLULAR AND EXTRACELLULAR CHANGES OF AMINO-ACIDS IN THE CEREBRAL-CORTEX OF THE NEONATAL RAT DURING HYPOXIC-ISCHEMIA
    ANDINE, P
    SANDBERG, M
    BAGENHOLM, R
    LEHMANN, A
    HAGBERG, H
    [J]. DEVELOPMENTAL BRAIN RESEARCH, 1991, 64 (1-2): : 115 - 120
  • [3] LOW-DOSES OF L-MONOSODIUM GLUTAMATE PROMOTE NEURONAL GROWTH AND DIFFERENTIATION INVITRO
    ARUFFO, C
    FERSZT, R
    HILDEBRANDT, AG
    CERVOSNAVARRO, J
    [J]. DEVELOPMENTAL NEUROSCIENCE, 1987, 9 (04) : 228 - 239
  • [4] PROGNOSIS OF NEWBORN-INFANTS WITH HYPOXIC-ISCHEMIC BRAIN INJURY ASSESSED BY PHOSPHORUS MAGNETIC-RESONANCE SPECTROSCOPY
    AZZOPARDI, D
    WYATT, JS
    CADY, EB
    DELPY, DT
    BAUDIN, J
    STEWART, AL
    HOPE, PL
    HAMILTON, PA
    REYNOLDS, EOR
    [J]. PEDIATRIC RESEARCH, 1989, 25 (05) : 445 - 451
  • [5] GLUTAMATE RECOGNITION SITES IN HUMAN-FETAL BRAIN
    BARKS, JD
    SILVERSTEIN, FS
    SIMS, K
    GREENAMYRE, JT
    JOHNSTON, MV
    [J]. NEUROSCIENCE LETTERS, 1988, 84 (02) : 131 - 136
  • [6] INOSITOL PHOSPHATES AND CELL SIGNALING
    BERRIDGE, MJ
    IRVINE, RF
    [J]. NATURE, 1989, 341 (6239) : 197 - 205
  • [7] PERINATAL HYPOXIC-ISCHEMIC BRAIN INJURY ENHANCES QUISQUALIC ACID-STIMULATED PHOSPHOINOSITIDE TURNOVER
    CHEN, CK
    SILVERSTEIN, FS
    FISHER, SK
    STATMAN, D
    JOHNSTON, MV
    [J]. JOURNAL OF NEUROCHEMISTRY, 1988, 51 (02) : 353 - 359
  • [8] ISCHEMIA DOES NOT INDUCE THE RELEASE OF EXCITOTOXIC AMINO-ACIDS FROM THE HIPPOCAMPUS OF NEWBORN RATS
    CHERICI, G
    ALESIANI, M
    PELLEGRINIGIAMPIETRO, DE
    MORONI, F
    [J]. DEVELOPMENTAL BRAIN RESEARCH, 1991, 60 (02): : 235 - 240
  • [9] THE ROLE OF GLUTAMATE NEUROTOXICITY IN HYPOXIC-ISCHEMIC NEURONAL DEATH
    CHOI, DW
    ROTHMAN, SM
    [J]. ANNUAL REVIEW OF NEUROSCIENCE, 1990, 13 : 171 - 182
  • [10] SELECTIVE SPARING OF NADPH-DIAPHORASE NEURONS IN NEONATAL HYPOXIA-ISCHEMIA
    FERRIERO, DM
    ARCAVI, LJ
    SAGAR, SM
    MCINTOSH, TK
    SIMON, RP
    [J]. ANNALS OF NEUROLOGY, 1988, 24 (05) : 670 - 676