Murine neocortical histogenesis is perturbed by prenatal exposure to low doses of bisphenol A

Journal of Neuroscience Research - Tập 84 Số 6 - Trang 1197-1205 - 2006
Keiko Nakamura1,2, Kyoko Itoh1, Takeshi Yaoi1, Yasuhiro Fujiwara1, Tohru Sugimoto2, Shinji Fushiki1
1Department of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan
2Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan

Tóm tắt

AbstractBisphenol A (BPA) has been shown to disrupt thyroid hormone function. We therefore studied whether prenatal exposure to low‐doses of BPA affects the morphology and the expression of some genes related to brain development in the murine fetal neocortex. Pregnant mice were injected subcutaneously with 20 μg/kg of BPA daily from embryonic day 0 (E0). Control animals received vehicle alone. For evaluating cell proliferation, neuronal differentiation and migration, bromodeoxyuridine (BrdU) was injected intraperitoneally into pregnant mice with various regimens and the brains were processed for immunohistochemistry. The total RNA was extracted from the embryonic telencephalon at various embryonic stages. The BrdU‐labeled cells examined 1 hour after BrdU injection showed no differences between the BPA‐treated and control groups (n = 10, each), which indicated that the proliferation of precursor cells was not affected. The BrdU‐labeled cells, analysed 2 days after BrdU injection, were decreased in the ventricular zone of BPA‐treated mice at E14.5 and E16.5, whereas they were increased in the cortical plate at E14.5 as compared with those in control mice (n = 10, each). Furthermore, the expression of Math3, Ngn2, Hes1, LICAM, and THRα was significantly upregulated at E14.5 in the BPA‐treated group. These results suggested that BPA might disrupt normal neocortical development by accelerating neuronal differentiation/migration. © 2006 Wiley‐Liss, Inc.

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Journal of Neuroscience Research

Tập 84 Số 6

1197-1205

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