Relationships between γ‐aminobutyrate and succinate cycles during and after cerebral ischemia

Some metabolites (glycogen, glucose, glucose‐6‐phosphate, pyruvate, lactate, citrate, α‐ketoglutarate, succinate, fumarate, malate, glutamate, aspartate, γ‐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 γ‐aminobutyrate, and with the decrease of malate, fumarate, and α‐ketoglutarate. These events may be regarded as an expression of the activation of the γ‐aminobutyrate cycle and of the succinate cycle, where succinate itself, in the absence of O 2 , 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 γ‐aminobutyrate, as an expression of the possible activation of the γ‐glutamyl and γ‐aminobutyrate cycles during recovery.