31P]/[1H] nuclear magnetic resonance study of mitigating effects of GYKI 52466 on kainate-induced metabolic impairment in perfused rat cerebrocortical slices

Epilepsia
P TangY Xu

Abstract

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 potential mitigating effects of GYKI 52466 [1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine] in superfused rat cerebral cortical slices. Interleaved [31P]/[1H] magnetic resonance spectroscopy (MRS) was used to assess energy metabolism, intracellular pH (pHi), 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). In the absence of GYKI 52466 and during the KA exposure, NAA, PCr, and ATP levels were decreased to 91.1 +/- 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, was reduced from 7.27 +/- 0.02 to 7.13 +/- 0.02. During 4-h recovery with KA-free ACSF, pHi rapidly and Lac gradually recovered, NAA decreased further to 85.5 +/- 0.3%, and PCr and ATP showed little recovery. Removal of Mg2+ from ACSF during KA exposure caused a more profound Lac increase (to 147.1 +/...Continue Reading

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Citations

Sep 1, 2000·Journal of Neuroscience Methods·D Okada
Apr 24, 2015·Toxicological Sciences : an Official Journal of the Society of Toxicology·Serguei LiachenkoJoseph Hanig

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