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GYKI 52466 Blocks the Increase in Extracellular Glutamate Induced by Ischaemia

B Arvin, C Moncada, E Le Peillet, A Chapman, B S Meldrum

Neuroreport. 1992 Mar;3(3):235-8.

PMID: 1355369

Abstract:

In vivo microdialysis has been used to study the effect of pre- or post-ischaemic administration of the non-NMDA antagonist 1-(4-amino-phenyl)-4-methyl-7, 8-methyl-endioxyl-5H-2,3- benzodiazepine hydrochloride (GYKI 52466), on the increases in extracellular glutamate levels induced by 20 minutes of four vessel occlusion in rats. In control rats, ischaemia resulted in transient increases in glutamate (4 fold), aspartate (6 fold) and gamma-aminobutyric acid (GABA) (15 fold) and decreases in glutamine (0.5 fold). Intravenous administration of GYKI 52466 (10 mg kg-1 bolus followed by 10 mg kg-1 h-1 infusion) beginning 20 minutes prior to the induction of ischaemia abolished ischaemia-induced glutamate release without affecting the increases in aspartate and GABA and the decrease in glutamine. Administration of GYKI 52466 immediately post-ischaemia resulted in a more rapid return of glutamate levels to basal values.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP192065568 GYKI 52466 hydrochloride GYKI 52466 hydrochloride 192065-56-8 Price
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