Influence of hyperoxia (1 ATA) on mouse brain GABA, glutamate, and glutamine.

Breathing 100% oxygen at ambient pressure induces disorders in glutamate, GABA, and ammonia metabolism in the brain, beginning 30 min after exposure. The steep increase in glutamine content points to an enhanced metabolism of endogenous amino acids and a breakdown of protein, although the glutamate content is scarcely influenced during the first hours of exposure. The graph of glutamine increase proceeds nearly asymptotically after 24 h, which may be related to the permeability of blood brain barrier for glutamine. The initially fast increase in the GABA level attains a half-maximum augmentation after 2-4 h of exposure and a maximum value after 50 h, but then the graph of GABA slopes steeply downwards, and approximately linearly, until 74-76 h and finally, by 103 h, more gradually approaches control values. The increase in GABA level is discussed with regard to the physiological role of GABA as a homeostatic agent that connects oxidative metabolism with neuronal function. Glutamate, the precursor of glutamine as well as GABA, is affected by oxygen breathing with a "loss" of more than 6 micronmol/g wet wt. after 100 h of exposure. Functionally, this diminution may be correlated to the increase of GABA with respect to its anti-excitatory effect and a possible postsynaptic function of glutamine synthetase.