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Contralateral response of macrophages and astrocytes to injury in the cerebral hemisphere of 6‐day‐old rat following prenatal gamma irradiation
Author(s) -
Setkowicz Zuzanna,
Bień Ewa,
Janeczko Krzysztof
Publication year - 2004
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2003.12.001
Subject(s) - glial fibrillary acidic protein , pathology , lesion , immunohistochemistry , prenatal development , medicine , fetus , biology , pregnancy , genetics
Wistar pregnant rats were exposed to a single 1.0 Gy dose of gamma rays on gestational days 13, 15, 17 or 19 (E13, E15, E17 and E19, respectively). When offsprings of the irradiated females became 6‐day‐old, they received a mechanical injury of the cerebral hemisphere. One or 2 days after the injury, [ 3 H]thymidine was injected and the animals were perfused. Brain sections were processed for BSI‐B4 isolectin histochemistry or immunohistochemistry for glial fibrillary acidic protein (GFAP) or S‐100‐β protein and subjected to autoradiography to visualise proliferating and non‐proliferating macrophages or proliferating astrocytes. Significant changes in the contralateral response to injury related to the day of prenatal irradiation could be detected. The response was minimal following irradiations performed on E15 and E17. At those stages of prenatal development, the majority of cortical neurons with interhemispheric connections were formed. Therefore, irradiation‐induced reduction of the neurons might minimise transfer of pathogenic stimuli to contralateral areas via degenerating nerve fibbers. Consequently, the degree at which the contralateral glial response reflected reactive changes at the lesion site might also be minimal. Results of the present study do not show in detail mechanisms underlying the differences in the contralateral reactivity to injury. They, however, might be of importance to histopathological investigations using animal models of cerebral dysplasia.