Dietary phytoestrogens enhance spatial memory and spine density in the hippocampus and prefrontal cortex of ovariectomized rats

Luine, Victoria N.; Attalla, Sara; Mohan, Govini; Costa, Ana Beatriz; Frankfurt, Maya

doi:10.1016/j.brainres.2006.07.016

Cited by 75 publications

(65 citation statements)

References 22 publications

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“…Comparing data from the two studies shows that withdrawal of soy caused a Ϸ50% drop in CA1 spine synapse density, whereas synapse counts after estradiol supplementation were approximately the same in both studies (31). Thus, the difference in the apparent magnitude of estradiol effects between the two studies can be explained by the well established estrogenic action of diets containing crude soy meal (33). However, spine synapses in the CA3sl/sr and DGsm hippocampal areas appear to be less responsive to estradiol.…”

Section: Discussionmentioning

confidence: 77%

Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates

Leranth

Hajszán²,

Szigeti‐Buck

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

207

151

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Exposure measurements from several countries indicate that humans are routinely exposed to low levels of bisphenol A (BPA), a synthetic xenoestrogen widely used in the production of polycarbonate plastics. There is considerable debate about whether this exposure represents an environmental risk, based on reports that BPA interferes with the development of many organs and that it may alter cognitive functions and mood. Consistent with these reports, we have previously demonstrated that BPA antagonizes spine synapse formation induced by estrogens and testosterone in limbic brain areas of gonadectomized female and male rats. An important limitation of these studies, however, is that they were based on rodent animal models, which may not be representative of the effects of human BPA exposure. To address this issue, we examined the influence of continuous BPA administration, at a daily dose equal to the current U.S. Environmental Protection Agency's reference safe daily limit, on estradiol-induced spine synapse formation in the hippocampus and prefrontal cortex of a nonhuman primate model. Our data indicate that even at this relatively low exposure level, BPA completely abolishes the synaptogenic response to estradiol. Because remodeling of spine synapses may play a critical role in cognition and mood, the ability of BPA to interfere with spine synapse formation has profound implications. This study is the first to demonstrate an adverse effect of BPA on the brain in a nonhuman primate model and further amplifies concerns about the widespread use of BPA in medical equipment, and in food preparation and storage. monkey ͉ stereology ͉ synaptic plasticity S ince the 1950s, the synthetic xenoestrogen bisphenol A (BPA) has been used in the manufacture of plastics with a broad range of uses, including dental prostheses and sealants (1), the polycarbonate lining of metal cans used to preserve foods (2), baby bottles (3) and the clear plastic cages used to house laboratory animals (4). BPA also is used as an additive in many products. Its global production rate is Ͼ6 billion pounds per year. Polycarbonate is less durable than commonly believed, because the ester bond linking BPA molecules to the plastic can be hydrolyzed. With the rate of hydrolysis increasing dramatically under both acidic and basic conditions, and at elevated temperatures, BPA leaches out of polycarbonate containers into food and beverages under normal conditions of use (3-5). As a result, exposure measurement data from several countries, including the United States, indicate that humans are widely exposed to low levels of BPA on a continuous basis (6).There is considerable debate about whether this exposure represents an environmental risk, based mostly on the fact that some hormonally active chemicals exhibit radically different potencies in different bioassay systems, making it difficult to assess their potential adverse effects (7). For example, in a two-generation trial in rats, BPA was reported to not induce significant reproductive abnormalities at ...

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Section: Discussionmentioning

confidence: 77%

Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates

Leranth

Hajszán²,

Szigeti‐Buck

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

207

151

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“…The Golgi impregnation procedure was carried out using the FD Rapid GolgiStain kit (FD Neurotechnologies, Inc., Columbia, MD) as previously described (34,35). The apical and basal dendritic spine density of pyramidal cells in the medial PFC (layers II/III) and the CA1 region of the hippocampus were analyzed using a Nikon Eclipse E400 microscope (Nikon, Tokyo, Japan) and the Spot Advanced Program for Windows (version 3.5; Diagnostic Instruments, Inc., Sterling Heights, MI) as previously described (34,35). Counting was treatment blind for each dendrite segment, and spine density was determined as the number of spines divided by the length of the dendrite being measured.…”

Section: Golgi Impregnation and Spine Density Analysismentioning

confidence: 99%

Estrogen-Induced Memory Enhancements Are Blocked by Acute Bisphenol A in Adult Female Rats: Role of Dendritic Spines

2012

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Acute effects of bisphenol (BPA), an environmental chemical, on estradiol (17α or β-E2)-dependent recognition memory and dendritic spines in the medial prefrontal cortex and hippocampus were investigated in adult female rats. Ovariectomized rats received BPA 30 min before or immediately after a sample trial (viewing objects), and retention trials were performed 4 h later. Retention trials tested discrimination between old and new objects (visual memory) or locations (place memory). When given immediately after the sample trial, BPA, 1-400 μg/kg, did not alter recognition memory, but 1 and 40 μg/kg BPA, respectively, blocked 17β-E2-dependent increases in place and visual memory. When ovariectomized rats were tested with 17α-E2, 1 μg/kg BPA blocked place memory, but up to 40 μg did not block visual memory. BPA, given to cycling rats at 40 μg/kg, blocked visual, but not place, memory during proestrus when 2 h intertrial delays were given. Spine density was assessed at times of memory consolidation (30 min) and retention (4 h) after 17β-E2 or BPA + 17β-E2. In prefrontal cortex, BPA did not alter E2-dependent increases. In the hippocampus, BPA blocked E2 increases in basal spines at 4 h and was additive with E2 at 30 min. Thus, these novel data show that doses of BPA, below the current Environmental Protection Agency safe limit of 50 μg/kg, rapidly alter neural functions dependent on E2 in adult female rats.

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“…Object placement testing occurred 24 hours after open field testing and was similar to paradigms previously described (Beck and Luine, 2002;Luine et al, 2006;Wallace et al, 2006). Rats were placed in a corner of the open field apparatus and the starting position was counter-balanced among groups.…”

Section: Open Field and Object Placementmentioning

confidence: 99%

Assessment of estradiol influence on spatial tasks and hippocampal CA1 spines: Evidence that the duration of hormone deprivation after ovariectomy compromises 17β-estradiol effectiveness in altering CA1 spines

McLaughlin

Bimonte‐Nelson

Neisewander

et al. 2008

Hormones and Behavior

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Two pulses of 17β-estradiol (10µg) are commonly used to increase hippocampal CA1 apical dendritic spine density and alter spatial performance in ovariectomized (OVX) female rats, but rarely are the measures combined. The goal of this study was to use this two-pulse injection protocol repeatedly with intervening wash-out periods in the same rats to: 1) measure spatial ability using different tasks that require hippocampal function and 2) determine whether ovarian hormone depletion for an extended 10-week period reduces 17β-estradiol's effectiveness in elevating CA1 apical dendritic spine density. Results showed that two injections of 10µg 17β-estradiol (72 and 48 hrs prior to testing and timed to maximize CA1 apical spine density at behavioral assessment) corresponded to improved spatial memory performance on object placement. In contrast, two injections of 5µg 17β-estradiol facilitated spatial learning on the water maze compared to rats given two injections of 10µg 17β-estradiol or the sesame oil vehicle. Neither 17β-estradiol dose altered Y-maze performance. As expected, the intermittent two-pulse injection protocol increased CA1 apical spine density, but ten weeks of OVX without estradiol treatment decreased the effectiveness of 10µg 17β-estradiol to increase CA1 apical spine density. Moreover, two pulses of 5µg 17β-estradiol injected intermittently failed to alter CA1 apical spine density and decreased basal spine density. These results demonstrate that extended time without ovarian hormones reduces 17β-estradiol's effectiveness to increase CA1 apical spine density. Collectively, these findings highlight the complex interactions among estradiol, CA1 spine density/morphology, and task requirements, all of which contribute to behavioral outcomes.

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Dietary phytoestrogens enhance spatial memory and spine density in the hippocampus and prefrontal cortex of ovariectomized rats

Cited by 75 publications

References 22 publications

Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates

Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates

Estrogen-Induced Memory Enhancements Are Blocked by Acute Bisphenol A in Adult Female Rats: Role of Dendritic Spines

Assessment of estradiol influence on spatial tasks and hippocampal CA1 spines: Evidence that the duration of hormone deprivation after ovariectomy compromises 17β-estradiol effectiveness in altering CA1 spines

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