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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Intrauterine methylmercury intoxication. Consequence of the inherent brain lesions and cognitive dysfunction in

A Kakita1, K Wakabayashi, M Su

  • 1Department of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan. kakita@bri.niigata-u.ac.jp

Brain Research
|September 15, 2000
PubMed

We studied the effects of intrauterine neurotoxicity by methylmercury (MeHg) on the postnatal developing and adult stages of rats. We used offspring delivered from dams that had been given 1 mg/kg/day methylmercury chloride for 5 pregestational days and throughout pregnancy. Histopathological examination of the brains of a proportion of the offspring on postnatal days 1 (P1) and P3 revealed degenerative neurons in the brain stem and the limbic system, including the hippocampus and the amygdala. At P7 and P14, degenerative neurons were indiscernible, but reactive astrocytosis remained in the brain stem. At P70 and P180, the brains seemed to have developed well. However, in behavioral analyses performed at 6 months of age, MeHg-exposed rats showed a significant learning disability in the passive avoidance response compared with controls, but no differences in water maze performance. Furthermore, morphometric analysis of the amygdala and hippocampus revealed significantly fewer neurons in both areas in the MeHg-exposed rats. Thus, chronic intrauterine exposure to low-dose MeHg induces a decrease in neuron population in the limbic system, and the offspring have impaired higher brain function.

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