Changes in amino acids (AA) and ammonia were investigated in the cerebral cortex and striatum of rats after the following conditions: 1) one hyperbaric oxygen (HBO)-induced seizure (6 ATA O2); 2) exposure to 6 ATA air; and 3) exposure to atmospheric pressure (no seizures in both latter groups). Exposure to 6 ATA air produced no change with respect to atmospheric pressure. After HBO seizure, AA levels (except for gamma-amino butyric acid, GABA, and glutamine), with respect to 6 ATA air levels, were altered in the striatum with a concomitant rise in ammonia (+70%) at variance with the cortex. These changes could be explained by increased oxidative deamination in the striatum. Decrease in taurine content (-66%) in the striatum, where HBO lipoperoxidation exists, suggests an alteration of glial function leading to blockade of uptake and loss of released products in interstitial fluid. This pattern of change recalls the one seen in ischemic conditions, but cannot be confirmed in the absence of measurements of extracellular amino acid levels under HBO conditions. The maintenance in the level of GABA would favor its role in controlling seizure. In the cortex, only a few AA levels decreased, along with a nonsignificant trend for ammonia to increase. The remaining abnormalities in the striatum, after the first HBO seizure, may explain the already known repetition of seizures in continuously exposed animals and are consistent with previous data on the important role of the striatum.