Abstract
The dynamics of soluble AChE and BChE (EC 3.1.1.7; EC 3.1.1.8) in the hippocampus, cortex, cerebellum and blood serum of control rats and rats exposed to prenatal hypoxia was studied on days 5, 10 and 30 of postnatal development. The activity of soluble AChE in all brain structures was found to reach its maximum on postnatal day 10, either persisting then at this level (in the cerebellum and cortex) or decreasing by day 30 (in the hippocampus). Similar changes were found in the activity of BChE, which was roughly one level of magnitude lower than of AChE in all the brain structures studied in this work. Prenatal hypoxic exposure on day 14 of embryonic development led to statistically significant changes in the activity of soluble AChE and BChE in all the studied brain structures, as well as in blood serum. In rats exposed to prenatal hypoxia, serum AChE and BChE activities on postnatal days 5 and 10 were significantly lower while on day 30 indistinguishable from the control values. Thus, oxygen deficit in the maternal organism during pregnancy significantly affects the activity of soluble forms of the key enzymes of the central and peripheral cholinergic systems, indicating possible changes in the formation of these systems in early ontogenesis. This may lead both to impaired neurogenesis and malformation of the motor and cognitive functions and general homeostatic imbalance during animal and human development.
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