Relationships between gamma-aminobutyrate and succinate cycles during and after cerebral ischemia.
Some metabolites (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate, citrate, alpha-ketoglutarate, succinate, fumarate, malate, glutamate, aspartate, gamma-aminobutyrate, glutamine, alanine, NH+4) were measured in rat cerebral cortex after 5 minutes of complete compression ischemia, as well as after 5, 15, or 30 minutes of recirculation following 5 minutes of ischemia. Complete ischemia induced a drop of glycolytic substrates and intermediates, consistent with the increase of lactate, succinate, alanine, and gamma-aminobutyrate, and with the decrease of malate, fumarate, and alpha-ketoglutarate. These events may be regarded as an expression of the activation of the gamma-aminobutyrate cycle and of the succinate cycle, where succinate itself, in the absence of O2, acts as a terminal electron acceptor. During post-ischemic recovery, cerebral parameters tended to normalize, except for the further increase of alanine and the still higher than normal content of both succinate and gamma-aminobutyrate, as an expression of the possible activation of the gamma-glutamyl and gamma-aminobutyrate cycles during recovery.
D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D006019:Glycolysis; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013386:Succinates / Q000378:metabolism*; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D013386:Succinates; D005680:gamma-Aminobutyric Acid