Acute effects of estrogen and bisphenol -A, an environmental chemical, on cognitive and neural function
Item
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Title
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Acute effects of estrogen and bisphenol -A, an environmental chemical, on cognitive and neural function
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Identifier
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d_2009_2013:5df202a4bcfb:10357
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identifier
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10569
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Creator
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Inagaki, Tomoko,
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Contributor
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Victoria Luine
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Date
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2010
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Language
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English
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Publisher
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City University of New York.
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Subject
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Psychobiology | Behavioral psychology | Neurosciences | Estradiol | Hippocampus | Monoamines | Object recognition | Spatial memory | Spine density
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Abstract
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Many natural and synthetic chemicals in environment can mimic or antagonize the effects of endogenous hormones. Bisphenol A (BPA) is one such chemical, with mixed estrogen agonist/antagonist properties. Recent evidence indicates that estrogen and BPA may exert effects on brain functions not only through genomic but also through non-genomic pathways, activating membrane-associcated estrogen receptors. Because at present little is known about how acute BPA may interact with estrogen in the adult brain and affect estrogen mediated behaviors such as memory and learning, this research examined acute effects of estradiol (E2) and BPA, alone, and in combination, on behavior (memory consolidation) and neural function (spine density and monoamine levels) in adult ovariectomized female rats. For behavioral study, acute 17beta- and 17alpha-E2 treatment effects on spatial and non-spatial memory consolidation were tested using object placement (OP) and object recognition (OR) tasks. Both isomers of estradiol facilitated memory consolidation, but enhancement occurred in a time-, dose-, and task specific manner. The dose-response relationship was an inverted-U for both tasks. Co-administration of BPA blocked E2-induced OP memory enhancement far below the current reference safe dose of 50microg/kg/day. A larger BPA dose was needed to block 17a-E2 induced OR memory enhancement. BPA alone had no effect on OP memory, but high doses enhanced OR memory.;To examine possible neural systems that may contribute to acute E2 and BPA treatment effects, brains were removed for neuromorphological and neurochemical analysis. Golgi impregnation 30 minutes after acute treatments showed that E2 increased apical and basal dendritic spine density in pyramidal neurons of of the prefrontal cortex (PFC), and basal, but not apical, spine density in pyramidal neurons of CA1 region of the hippocampus. Co-administration of BPA with E2 further increased apical and basal spine density in both the PFC and the CA1. Golgi impregnation 4 hours after acute treatments found that co-administration of BPA significantly suppressed E2-induced basal CA1spine density. Neurochemical analyses revealed that acute estrogen increased monoamine and metabolite levels in the PFC, but decreased these chemicals in the hippocampus. Co-administration of BPA further increased monoamine and metabolite concentrations in the PFC.;In summary, the current data provide new information about acute effects of estrogen and BPA on memory and brain function. BPA interacts with E2 at very low doses, and rapidly alters behavioral and neural response to E2. These findings demonstrate BPA behavioral changes at very low doses in the membrane environment and suggest low level exposure of BPA may have a powerful, negative impact, rapidly altering behavioral and neural responses to endogenous estrogen.
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Type
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dissertation
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Source
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2009_2013.csv
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degree
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Ph.D.
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Program
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Psychology
