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Low circulating levels of bisphenol‐A induce cognitive deficits and loss of asymmetric spine synapses in dorsolateral prefrontal cortex and hippocampus of adult male monkeys
Author(s) -
Elsworth John D.,
Jentsch James D.,
Groman Stephanie M.,
Roth Robert H.,
Redmond Eugene D.,
Leranth Csaba
Publication year - 2015
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.23735
Subject(s) - hippocampus , prefrontal cortex , dorsolateral prefrontal cortex , endocrine system , neuroscience , dendritic spine , endocrine disruptor , psychology , hippocampal formation , cognition , population , endocrinology , medicine , hormone , environmental health
Bisphenol‐A (BPA) is widely used in the manufacture of plastics, epoxy resins, and certain paper products. A majority of the population in the developed world is routinely exposed to BPA from multiple sources and has significant circulating levels of BPA. Although BPA is categorized as an endocrine disruptor with a growing literature on adverse effects, it is uncertain whether cognitive dysfunction is induced in humans by exposure to BPA. The present study examined the impact of BPA in primate brain by exposing adult male vervet monkeys for 4 weeks continuously to circulating levels of BPA that were in the range measured in studies of humans environmentally exposed to BPA. This regimen of exposure to BPA decreased both working memory accuracy and the number of excitatory synaptic inputs on dendritic spines of pyramidal neurons in two brain regions that are necessary for working memory (prefrontal cortex and hippocampus). These observed behavioral and synaptic effects were ameliorated following withdrawal from BPA. As Old World monkeys (e.g., vervets) and humans share some uniquely primate morphological, endocrine, and cognitive traits, this study indicates the potential for significant cognitive disruption following exposure of humans to BPA. J. Comp. Neurol. 523:1248–1257, 2015. © 2015 Wiley Periodicals, Inc.