Ascorbic acid was repeatedly monitored in vivo in the striatum of rats subjected to an increasing pressure (100 bar/h compression rate; 0.5 bar partial pressure of O2 He-O2 mixture, up to 120 bar (121 ATA), to which they were exposed for 1 h. Measurements were performed using differential pulse voltammetry and carbon fiber microelectrodes. High-pressure-exposed animals exhibited a dramatic decrease of striatal ascorbic acid. This decrease was detectable at pressures as low as 50 bar and significant over 70 bar (75% of the control level), and the lower level (25% of the control level) was reached shortly after the end of the compression period. This finding is discussed in relation to the physiological role of ascorbic acid in the brain, e.g., its participation in the defense mechanisms against reactive O2 intermediates and lipid peroxidations and its probable involvement in neurotransmission. Emphasis is placed on a possible increased sensitivity of nerve cell membrane phospholipids to peroxidation under stressful hyperbaric situations.