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Titolo:
[P-31] [H-1] NUCLEAR-MAGNETIC-RESONANCE STUDY OF MITIGATING EFFECTS OF GYKI-52466 ON KAINATE-INDUCED METABOLIC IMPAIRMENT IN PERFUSED RAT CEREBROCORTICAL SLICES/
Autore:
TANG P; LIACHENKO S; MELICK JA; XU Y;
Indirizzi:
UNIV PITTSBURGH,DEPT ANESTHESIOL & CRIT CARE MED,W-1358 BIOMED SCI TOWER PITTSBURGH PA 15261 UNIV PITTSBURGH,DEPT ANESTHESIOL & CRIT CARE MED PITTSBURGH PA 15261 UNIV PITTSBURGH,DEPT PHARMACOL PITTSBURGH PA 15261
Titolo Testata:
Epilepsia
fascicolo: 6, volume: 39, anno: 1998,
pagine: 577 - 583
SICI:
0013-9580(1998)39:6<577:[[NSOM>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
STATUS EPILEPTICUS; KAINIC ACID; INTRACELLULAR PH; ANTICONVULSANT ACTIVITY; RECEPTOR RESPONSES; GLUTAMATE RELEASE; HIPPOCAMPUS; SEIZURES; BRAIN; HYPERCAPNIA;
Keywords:
BRAIN SLICE; STATUS EPILEPTICUS; EXCITOTOXICITY; GYKI 52466; KAINIC ACID; NUCLEAR MAGNETIC RESONANCE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
P. Tang et al., "[P-31] [H-1] NUCLEAR-MAGNETIC-RESONANCE STUDY OF MITIGATING EFFECTS OF GYKI-52466 ON KAINATE-INDUCED METABOLIC IMPAIRMENT IN PERFUSED RAT CEREBROCORTICAL SLICES/", Epilepsia, 39(6), 1998, pp. 577-583

Abstract

Purpose: Kainic acid (KA) has long been used in experimental animals to induce status epilepticus (SE), A mechanistic implication of this is the association between excitotoxicity and brain damage during or after SE. We evaluated KA-induced metabolic impairment and the potentialmitigating effects of GYKI 52466 4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine] in superfused rat cerebral cortical slices. Methods: Intel leaved [P-31]/[H-1] magnetic resonance spectroscopy (MRS) was usedto assess energy metabolism, intracellular pH (pH(i)), N-acetyl-L-aspartate (NAA) level, and lactate (Lac) formation before, during, and after a 56-min exposure to 4 mM KA in freshly oxygenated artificial cerebrospinal fluid (oxy-ACSF). Results: In the absence of GYKI 52466 and during the KA exposure, NAA, PCr, and ATP levels were decreased to 91.1 rt 0.8, 62.4 +/- 3.9, and 59.1 +/- 4.3% of the control, respectively; Lac was increased to 118.2 +/- 2.1%, and pH(i) was reduced from 7.27+/- 0.02 to 7.13 +/- 0.02. During 4-h recovery with KA-free ACSF, pH(i) rapidly and Lac gradually recovered, NAA decreased further to 85.5 /- 0.3%, and PCr and ATP showed little recovery. Removal of Mg2+ fromACSF during KA exposure caused a more profound Lac increase (to 147.1+/- 4.0%) during KA exposure and a further NAA decrease (to 80.4 +/- 0.5%) during reperfusion, but did not exacerbate PCr, ATP, and pH(i) changes. Inclusion of 100 mu M GYKI 52466 during KA exposure significantly improved energy metabolism: the PCr and ATP levels were above 76.6+/- 2.1 and 82.0 +/- 2.9% of the control, respectively, during KA exposure and recovered to 101.4 +/- 2.4 and 95.0 +/- 2.4%, respectively, during reperfusion. NAA level remained at 99.8 +/- 0.6% during exposure and decreased only slightly at a later stage of reperfusion. Conclusions: Our finding supports the notion that KA-induced SE causes metabolic disturbance and neuronal injury mainly by overexcitation through non-N-methyl-D-aspartate (NMDA) receptor functions.

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Documento generato il 05/04/20 alle ore 13:18:00