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
| Autor: | Robert H. Roth, James David Jentsch, Stephanie M. Groman, John D. Elsworth, Eugene Redmond, Csaba Leranth |
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| Rok vydání: | 2015 |
| Předmět: |
endocrine system
medicine.medical_specialty education.field_of_study Dendritic spine biology urogenital system Working memory General Neuroscience Population Hippocampus Dorsolateral prefrontal cortex medicine.anatomical_structure Endocrinology Endocrine disruptor Internal medicine biology.animal medicine Primate education Prefrontal cortex Neuroscience hormones hormone substitutes and hormone antagonists |
| Zdroj: | Journal of Comparative Neurology. 523:1248-1257 |
| ISSN: | 0021-9967 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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