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Neil J. MacLusky,¹ Tibor Hajszan,^2,3 and Csaba Leranth^2,4

¹Center for Neural Recovery and Rehabilitation Research, Helen Hayes Hospital, New York, New York, USA; ²Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut, USA; ³Laboratory of Molecular Neurobiology, Biological Research Center, Hungarian Academy of Sciences, Szeged, Hungary; ⁴Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut, USA

Abstract
Bisphenol A (BPA) is an estrogenic chemical that is widely used in the manufacture of plastics and epoxy resins. Because BPA leaches out of plastic food and drink containers, as well as the BPA-containing plastics used in dental prostheses and sealants, considerable potential exists for human exposure to this compound. In this article we show that treatment of ovariectomized rats with BPA dose-dependently inhibits the estrogen-induced formation of dendritic spine synapses on pyramidal neurons in the CA1 area of the hippocampus. Significant inhibitory effects of BPA were observed at a dose of only 40 µg/kg, below the current U.S. Environmental Protection Agency reference daily limit for human exposure. Because synaptic remodeling has been postulated to contribute to the rapid effects of estrogen on hippocampus-dependent memory, these data suggest that environmental BPA exposure may interfere with the development and expression of normal sex differences in cognitive function, via inhibition of estrogen-dependent hippocampal synapse formation. It may also exacerbate the impairment of hippocampal function observed during normal aging, as endogenous estrogen production declines. Key words: bisphenol A, CA1, estradiol, hippocampus, spine synapse density. Environ Health Perspect 113:675-679 (2005) . doi:10.1289/ehp.7633 available via http://dx.doi.org/ [Online 24 February 2005]

Address correspondence to N.J. MacLusky, Center for Neural Recovery and Rehabilitation Research, Helen Hayes Hospital, New York State Department of Health, Route 9W, West Haverstraw, NY 10993-1195 USA. Telephone: (845) 786-4810. Fax: (845) 786-4875. E-mail: macluskyn@helenhayeshosp.org

We thank K. Szigeti-Buck and G. Thomas for excellent technical assistance.

This work was supported by National Institutes of Health grants MH60858 and NS42644 (C.L.) and a Dow Chemical SPHERE award (N.J.M.) .

N.J.M. received a Dow Chemical SPHERE award, an unrestricted award that provided support to the research laboratory but no direct compensation to the author. T.H. and C.L. declare they have no competing financial interests.

Received 4 October 2004 ; accepted 24 February 2005.