Autor: |
Miyagawa K; Department of Toxicology, Hoshi University School of Pharmacy and Pharmaceutical Sciences., Narita M, Narita M, Niikura K, Akama H, Tsurukawa Y, Suzuki T |
Jazyk: |
angličtina |
Zdroj: |
Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology [Nihon Shinkei Seishin Yakurigaku Zasshi] 2007 Apr; Vol. 27 (2), pp. 69-75. |
Abstrakt: |
In the previous study, we reported that exposure to bisphenol-A induced the potentiation of dopamine receptor functions in the mouse limbic area, resulting in supersensitivity to methamphetamine-induced pharmacological actions. The present study was undertaken to investigate whether prenatal exposure to bisphenol-A could produce morphological change in dopaminergic neuron and the pattern of expression of genes regulating the dopaminergic neuron development. Here we found that prenatal and neonatal exposures to bisphenol-A increased the tyrosine hydroxylase- and dopamine transporter-like immunoreactivities in the adult mouse limbic area. The present molecular biological study shows that chronic bisphenol-A treatment produced a significant decrease in the dopaminergic neuron development factors, sonic hedgehog and glial cell line-derived neurotrophic factor, which were also decreased by prenatal exposure to bisphenol-A. These results suggest that chronic exposure to bisphenol-A could disrupt the dopaminergic neurotransmission in the process of dopaminergic neuron development. |
Databáze: |
MEDLINE |
Externí odkaz: |
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