Cell proliferation correlates with the postconceptual and not with the postnatal age in the hippocampal dentate gyrus, temporal neocortex and cerebellar cortex of preterm infants.
BACKGROUND: In previous studies, lower IQ scores and educational difficulties of preterm children were correlated with the reduced size of several brain areas, including the cerebellum and the hippocampus. The most plausible reason for reduction would be the reduced cell formation following premature birth. However, no data are available about the rate of postnatal cell proliferation in the different brain areas of preterms. METHODS: Cytoarchitectonics and cell proliferation were examined in the cerebellum, hippocampal formation and temporal neocortex of preterm infants who lived for several weeks or months. Cell proliferation was detected with Ki-67 immunostaining and proliferating cells were identified with vimentin as glial and with CD31 and periodic acid-Schiff (PAS) reaction as endothelial elements. RESULTS: The rate of cell formation and the width of the cytoarchitectonic layers of the cerebellum of preterm infants corresponded to that of the age-matched controls. In the hippocampal dentate gyrus, the rate of cell formation and the density of proliferating cells were slightly higher in the preterm infants than in the full-term age-matched controls. Endothelial cell proliferation and the surface area of the capillaries were larger in the dentate gyrus of preterms than in age-matched controls. CONCLUSION: Rate of cell proliferation that correlates with the postconceptual age is not reduced in preterms, therefore the reduced size of the cerebellum and hippocampal formation is unlikely to be the result of decreased cell formation.[1]References
- Cell proliferation correlates with the postconceptual and not with the postnatal age in the hippocampal dentate gyrus, temporal neocortex and cerebellar cortex of preterm infants. Abrahám, H., Tornóczky, T., Kosztolányi, G., Seress, L. Early Hum. Dev. (2004) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
