Neurochemical indices of rat-pups exposed to high hypoxia during critic period of prenatal development were studied in postnatal ontogenesis (on 17th day). It was revealed that serotonin shortage in the CNS structures of the intrauterinly stressed rat-pups can lead to embryo’s death or to pathology of brain structures as a result.
The findings obtained in postnatal ontogenesis showed decreasing in 5-hydroxytryptophan decarboxylase activity by 29% in the cortical tissues which makes 0.106±0.004 (in control – 0.150±0.005 µmol serotonin/g·h); in the cerebellum – by 14% - 0.074±0.030 (in control – 0.086±0.003 µmol serotonin/g·h), in the brain stem – by 45% – 0.183±0.003 (in control – 0.331±0.004 µmol serotonin/g·h) and in hypothalamus by 37% – 0.250±0.001 (in control – 0.396±0.004 µmol serotonin/g·h) in 17-days rat-pups exposed to high hypoxia during 13-16 days of prenatal development (during implantation period of prenatal development).
As seen from the findings in 17-day male rat-pups exposed to hypoxia during intrauterine period of prenatal ontogenesis 5-hydroxytryptophan decarboxylase activity in the structures was decreased by 14-45%.
Our studies indicate that 20 minute exposition of pregnant rats to hypoxia disturbs the development of the nervous system of the progeny. Exposure to hypoxia of embryos during the period of differentiation and migration of neuroblasts in the CNS structures caused the decrease in the 5-hydroxytryptophan decarboxylase activity by 14-45% in the studied structures of 17-day male rat-pups.
Decreasing of the enzyme in nervous structures of 17-day progeny owing to prenatal hypoxia appears proceeding of protein structures of the enzyme and its coenzyme – pyridoxal-5-phosphate.