0022-0930/03/3902-0203$25.00 © 2003 MAIK “Nauka/Interperiodica” Journal of Evolutionary Biochemistry and Physiology, Vol. 39, No. 2, 2003, pp. 203—210. Translated from Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, Vol. 39, No. 2, 2003, pp. 154—159. Original Russian Text Copyright © 2003 by Lavrenova, Nalivaeva, Zhuravin. COMPARATIVE AND ONTOGENIC PHYSIOLOGY Activity of Acetylcholinesterase in the Motor-Sensory Cortex in Early Ontogenesis of Rats Exposed to Prenatal Hypoxia S. M. Lavrenova, N. N. Nalivaeva, and I. A. Zhuravin Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia Received December 27, 2001 Abstract—Effects of acute prenatal hypoxia (13–14 days of gestation, 3 h, O 2 = 7%) on acetylcholinest- erase (AChE, EC 3.1.1.7) activity in homogenates, synaptosomes, and cytosol of the motor-sensory cortex of Wistar rats were studied on the days 1, 5, 10, 19 and 30 after birth. In homogenates of normally developing cortex, the AChE activity did not significantly change with age. Activity of AChE in synap- tosomes increased 4 times throughout the entire period of observation, while in the cytosol, 4.3 times to reach maximum at the 19th day. Maximum rise of the AChE activity in synaptosomes was observed at the period from the 5th to the 10th day. Activity of AChE in homogenate and synaptosomes of rats submitted to prenatal hypoxia decreased during the first five days after birth ( p < 0.001) but later, starting from the day 10, it increased in all fractions. A statistically significantly higher activity of AChE than in controls was revealed in homogenate of the motor-sensory cortex on day 19 ( p < 0.01), while in synaptosomes, on the days 19 and 26 ( p < 0.001 and p < 0.05, respectively), and in cytosol, on the days 10, 26, and 30 ( p < 0.05, p < 0.05, and p < 0.001). Maximum change in the ratio of AChE activities in cytosol and synaptosomes was found on the day 19 ( p < 0.01). At the same period of development, changes in the ratio of AChE activity in synaptosomes and homogenate of the control and hypoxic animals were also observed. Thus, prenatal hypoxia leads to in changes in the activity both of the cytosol and synaptosomal membrane-bound forms of AChE in the motor-sensory cortex of rats, which agrees with our own and literature data on disorder of neuro- and neuritogenesis in the process of formation of CNS and of behavioral reactions in early postnatal ontogenesis under the effect of pathogenic factors at certain days of prenatal ontogenesis. INTRODUCTION Prenatal hypoxia is one of the causes of disor- ders of normal brain development and formation of neurological functions at various stages of onto- genesis [1–4]. Animals subjected to prenatal hy- poxia have been revealed to get destructive changes in motor-sensory cortex [5], defective formation of motor reactions and impaired cognitive abilities at postnatal period of development [2–4]. Mecha- nisms of the effects of prenatal hypoxia are not yet well understood; however, it can be believed that the processes of disorders of the brain of embryos and adult animals there have common features under effects of hypoxia. Hypoxia was shown to be accompanied by an increased synthesis of active oxygen forms as well as by activation of lipid perox- idation, increased concentrations of intracellular calcium ions and a decreased activity of Na + ,K + - ATPase both in adult animals and embryos [6–10]. Meanwhile, it is only at the embryonic period that an intensive proliferation of nerve tube cells takes place, so the action of pathogenic factors at this pe- riod might lead to disorder of architecture of the motor-sensory cortex and other brain structures in postnatal ontogenesis of animals [5].