ИСТИНА

Introduction: Epilepsy is a major neurological disorder. Experimental and clinical data associates the higher seizure susceptibility with impaired oxygenation during the prenatal period. Prenatal hypoxia is a particular case of stress response. There have been no studies so far of the influence of acute hypobaric hypoxia on absence epilepsy. Absence epilepsy is a particular epileptic syndrome characterized by generalized non-convulsive seizures concomitant with a cessation of activity and associated with a transient alteration of consciousness. The goal of our study was to examine whether prenatal acute hypobaric hypoxia influences the development of absence epilepsy and changes seizure susceptibility of adult brain of rats. Methods: On day 14 of pregnancy (embryonic day 14 (E14)) six female WAG/Rij rats with spontaneous spike and wave discharges (SWDs) (9-11 Hz) were exposed to hypobaric hypoxia at 5% O2 (11500 m altitude, 145 mm Hg) in a decompression (altitude) chamber of 3.3 L volume. After closing the chamber, the air pressure inside decreased progressively during 1 min (200 m/sec) by the vacuum pump connected to the chamber. Six female WAG/Rij rats were not exposed to hypobaric hypoxia as control offspring. All male rat offspring (n=15) (control and experimental) at the age of 6 month were equipped with recording stainless-steel electrodes placed bilaterally over the frontal cortex. Baseline EEG was recorded for 4 hours. After that seizure susceptibility by injection i.p. of pentylenetetrazole (PTZ) - GABA-a receptor antagonist in dose 25 mg/kg 3 times every 15 min was tested. The mean duration and number of SWDs, spectral power density of SWDs evaluated by Welch method using FFT was analyzed in baseline EEG and mean duration of PTZ induced discharges were calculated. Results and discussion: In the rats of the experimental group, we observed a significant increase of mean duration of SWDs as compared to the control. No significant changes of number of SWDs were found. Our results showed that prenatal hypoxia does not effect spectral power density of SWDs. PTZ treatment induced a significant increase in mean duration of PTZ-induced discharges in comparison to control. The mean duration of seizures was longer in the experimental rats as compared to the control. Thus in the present study, it has been shown that prenatal acute hypobaric hypoxia has delayed effects on development of absence epilepsy. Prenatal hypoxia not only increased mean duration of SWDs, but also increased seizure susceptibility of adult brain of rats. We can suggest that no changes of number of SWDs means no changes in the perioral zone of somatosensory cortex where absence seizures are initiated. Also the delayed effect of acute hypobaric hypoxia is due to changes of the functions of hypothalamus-pituitary-adrenal system. Thus, acute hypobaric hypoxia as prenatal stress causes aggravation of absence epilepsy and enhance seizure susceptibility in WAG/Rij rats.