DIPHENYLHYDANTOIN ATTENUATES HYPOXIA-INDUCED RELEASE OF [H-3] GLUTAMATE FROM RAT HIPPOCAMPAL SLICES

被引：18

作者：

POTTER, PE

DETWILER, P

THORNE, B

MOSKAL, JR

机构：

[1] MONTEFIORE MED CTR,ALBERT EINSTEIN COLL MED,DEPT NEUROSURG,BRONX,NY 10467

[2] CHICAGO INST NEUROSURG & NEURORES,CHICAGO,IL 60614

来源：

BRAIN RESEARCH | 1991年 / 558卷 / 01期

关键词：

DIPHENYLHYDANTOIN; GLUTAMATE; HIPPOCAMPUS; HYPOXIA; ISCHEMIA; PHENYTOIN; STROKE;

D O I：

10.1016/0006-8993(91)90728-E

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The ability of diphenylhydantoin (DPH) to prevent hypoxia-induced [H-3]glutamate release was examined in perfused rat hippocampal slices. Hypoxia (25 min; 95% N2/5% CO2) caused a prolonged release of [H-3]glutamate, which was reduced significantly if DPH (20-mu-M) was present from the beginning of the perfusion. Perfusion with oxygenated medium (reoxygenation) following hypoxia also caused a pronounced release of glutamate. A therapeutic concentration of DPH, added before, during, or after hypoxia, decreased this release of glutamate. These results suggest that DPH may protect against glutamate-mediated neurotoxicity associated with stroke.

引用

收藏

页码：127 / 130

页数：4

相关论文

共 12 条

[1] ELEVATION OF THE EXTRACELLULAR CONCENTRATIONS OF GLUTAMATE AND ASPARTATE IN RAT HIPPOCAMPUS DURING TRANSIENT CEREBRAL-ISCHEMIA MONITORED BY INTRACEREBRAL MICRODIALYSIS [J].

BENVENISTE, H ;

DREJER, J ;

SCHOUSBOE, A ;

DIEMER, NH .

JOURNAL OF NEUROCHEMISTRY, 1984, 43 (05) :1369-1374

[2] EFFECTS OF ANOXIA ON THE STIMULATED RELEASE OF AMINO-ACID NEUROTRANSMITTERS IN THE CEREBELLUM INVITRO [J].

BOSLEY, TM ;

WOODHAMS, PL ;

GORDON, RD ;

BALAZS, R .

JOURNAL OF NEUROCHEMISTRY, 1983, 40 (01) :189-201

[3] THE EFFECTS OF CONVULSANT AND ANTI-CONVULSANT DRUGS ON THE RELEASE OF RADIOLABELED GABA, GLUTAMATE, NORADRENALINE, SEROTONIN AND ACETYLCHOLINE FROM RAT CORTICAL SLICES [J].

DEBOER, T ;

STOOF, JC ;

VANDUIJN, H .

BRAIN RESEARCH, 1982, 253 (1-2) :153-160

[4] EFFECT OF ISCHEMIA ON THE INVIVO RELEASE OF STRIATAL DOPAMINE, GLUTAMATE, AND GAMMA-AMINOBUTYRIC ACID STUDIED BY INTRACEREBRAL MICRODIALYSIS [J].

GLOBUS, MYT ;

BUSTO, R ;

DIETRICH, WD ;

MARTINEZ, E ;

VALDES, I ;

GINSBERG, MD .

JOURNAL OF NEUROCHEMISTRY, 1988, 51 (05) :1455-1464

[5] ISCHEMIA-INDUCED SHIFT OF INHIBITORY AND EXCITATORY AMINO-ACIDS FROM INTRACELLULAR TO EXTRACELLULAR COMPARTMENTS [J].

HAGBERG, H ;

LEHMANN, A ;

SANDBERG, M ;

NYSTROM, B ;

JACOBSON, I ;

HAMBERGER, A .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1985, 5 (03) :413-419

[6] CA-2+-DEPENDENT AND CA-2+- INDEPENDENT GLUTAMATE RELEASE, ENERGY STATUS AND CYTOSOLIC FREE CA-2+ CONCENTRATION IN ISOLATED NERVE-TERMINALS FOLLOWING METABOLIC INHIBITION - POSSIBLE RELEVANCE TO HYPOGLYCEMIA AND ANOXIA [J].

KAUPPINEN, RA ;

MCMAHON, HT ;

NICHOLLS, DG .

NEUROSCIENCE, 1988, 27 (01) :175-182

[7] CRITERIA FOR THE IDENTIFICATION OF CENTRAL NEUROTRANSMITTERS, AND THEIR APPLICATION TO STUDIES WITH SOME NERVE-TISSUE PREPARATIONS INVITRO [J].

ORREGO, F .

NEUROSCIENCE, 1979, 4 (08) :1037-1057

[8] TEMPORAL PROFILE OF NEURONAL DAMAGE IN A MODEL OF TRANSIENT FOREBRAIN ISCHEMIA [J].

PULSINELLI, WA ;

BRIERLEY, JB ;

PLUM, F .

ANNALS OF NEUROLOGY, 1982, 11 (05) :491-498

[9] K+ EFFLUX PATHWAYS AND NEUROTRANSMITTER RELEASE ASSOCIATED TO HIPPOCAMPAL ISCHEMIA - EFFECTS OF GLUCOSE AND OF K+ CHANNEL BLOCKERS [J].

SCHAEFFER, P ;

LAZDUNSKI, M .

BRAIN RESEARCH, 1991, 539 (01) :155-158

[10] 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