The aim of the present work was to study the long-term consequences of acute normobaric hypoxia during the perinatal period on the establishment of the hippocampal formation in rats. The experiments showed that hypoxia on day 2 of postnatal development led to significant damage to the structure of the hippocampal field, which showed different levels of sensitivity to the harmful factor. On day 20, all fields showed cell death and depletion of the pyramidal cell layers. The most marked neuron death occurred in fields CA4 and CA3. On day 30, a significant level of neuron death persisted in field CA4, though it decreased in field CA3 and was not seen in field CA1; neuron death in the granule layer of the dentate fascia increased. In addition, there were decreases in the sizes of pyramidal neuron bodies in all hippocampal fields. All hippocampal fields also showed activation of astrocyte reactions, which was more marked in field CA4, where gliosis persisted to prepubertal age (30 days).
hippocampus perinatal hypoxia cell death neuron size astrocyte reaction.
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D. E. Korzhevskii, I. P. Grigoriev, and V. A. Otellin, “Use of dehydrated fixatives containing zinc salts in neurohistological studies,” Morfologiya, 129, No. 1, 85–87 (2006).Google Scholar
W. F. Chen, H. Chang, L. T. Huang, et al., “Alterations in long-term seizure susceptibility and the complex of PSD-95 with NMDA receptor from animals previously exposed to perinatal hypoxia,” Epilepsia, 47, No. 2, 288–296 (2006).PubMedCrossRefGoogle Scholar
W. F. Chen, H. Chang, C. S. Wong, et al., “Impaired expression of postsynaptic density proteins in the hippocampal CA1 region of rats following perinatal hypoxia,” Exp. Neurol., 204, No. 1, 400–410 (2007).PubMedCrossRefGoogle Scholar
J. L. Daval, G. Pourié, G. Grojean, et al., “Neonatal hypoxia triggers transient apoptosis followed by neurogenesis in the rat CA1 hippocampus,” Pediatr. Res., 55, No. 4, 561–567 (2004).PubMedCrossRefGoogle Scholar
V. Louzoun-Kaplan, M. Zuckerman, J. R. Perez-Polo, and H. M. Golan, “Prenatal hypoxia downregulates the GABA pathway in newborn mice cerebral cortex; partial protection by MgSO4,” Int. J. Dev. Neurosci., 26, No. 1, 77–85 (2008).PubMedCrossRefGoogle Scholar
J. N. Nuñez, J. J. Ait, and M. M. McCarthy, “A novel model for prenatal brain damage. II. Long-term deficits in hippocampal cell number and hippocampal-dependent behavior following neonatal GABAA receptor activation,” Exp. Neurol., 181, No. 2, 270–280 (2003).PubMedCrossRefGoogle Scholar
L. Raman, I. Tkac, K. Ennis, et al., “In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus,” Brain Res., 156, No. 2, 202–209 (2005).CrossRefGoogle Scholar
Z. Simonová, K. Sterbová, G. Brozek, et al., “Postnatal hypobaric hypoxia in rats impairs water maze learning and the morphology of neurones and macroglia in cortex and hippocampus,” Behav. Brain Res., 141, No. 2, 195–205 (2003).PubMedCrossRefGoogle Scholar
S. V. Sizonenko, E. Sirimanne, Y. Mayell, et al., “Selective cortical alteration after hypoxic-ischemic injury in the very immature rat brain,” Pediatr. Res., 54, No. 2, 263–269 (2003).PubMedCrossRefGoogle Scholar
1.Laboratory for Nervous System Ontogeny (Director: Corresponding Member of the Russian Academy of Medical Sciences Professor V. A. Otellin), I. P. Pavlov Institute of PhysiologyRussian Academy of SciencesSt. PetersburgRussia