No symptoms related to central nervous system (CNS) oxygen toxicity have been reported when diving with oxygen rebreathers at depths shallower than 3 msw. We hypothesised that recovery from CNS oxygen toxicity will take place when the PO(2) is less than 130 kPa. We exposed rats to a high PO(2) (mainly 608 kPa) to produce CNS oxygen toxicity. The latency to the first electrical discharge (FED) preceding convulsions was determined as the animal's control latency. Thereafter, the rat was exposed to the same PO(2) for 60% of its latency, then to a lower PO(2) for 15 min (sufficient time for full recovery in normoxia), and finally to the high PO(2) again until appearance of the FED. If recovery from CNS oxygen toxicity takes place during the interim period, the latency for the final exposure to the high oxygen pressure should not be shorter than the control. The latencies to CNS oxygen toxicity for exposure to the high oxygen pressure after a 15-min interim period at 21, 101, 132, 203, 304, 405, and 456 kPa were 110, 110, 125, 94, 85, 54 and 38% of the control value, respectively. Only after the last two interim pressures were the latencies significantly shorter than control values. The remaining latencies were not significantly different from 100%. Recovery from CNS oxygen toxicity in the rat takes place at a PO(2) anywhere between 21 and 304 kPa. The present findings support our previous suggestion that recovery from CNS oxygen toxicity in humans will take place at a PO(2) below 130 kPa. If our findings are corroborated by further human studies, this will justify including recovery in the algorithm for CNS oxygen toxicity in closed-circuit oxygen divers.