The study of functions of the body in hypoxia is interesting because any pathological state may be accompanied by hypoxia, the depth of which in many cases determines the severity and outcome of the pathological process. Acute hypoxia is known to cause seizures [11]. With lowering of the metabolic rate due to ischemia or hypoxia, excitability of nerve cells is increased and their responses to stimulation becomes excessive. However, this process is self-limiting, for the sharply increasing metabolic rate during the epileptic fit quickly exhausts the reserves of the nerve cells and they cease to respond to stimulation. The development of epilepsy after hypoxia may be due to selective degeneration of axon terminals arising from GABA-ergic neurons [12]. There is evidence that in some cases hypoxia has an inhibitory action on the development of seizures [9]. It has also been shown that adaptation to hypoxia depresses seizure manifestations in rats genetically predisposed to epilepsy, in response to acoustic stress [5], under the influence of metrazol [7] and of strychnine and penicillin [3], and that correlation exists between the resistance of rats to hypoxia and to the convulsant action of strychnine and penicillin [1]. The aim of this investigation was to study the effect of acute hypoxia on the development of metrazol seizures.