Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.

Eilam‐Stock, Tehila; Serrano, Peter A.; Frankfurt, Maya; Luine, Victoria N.

doi:10.1037/a0025959

Cited by 107 publications

(106 citation statements)

References 85 publications

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“…[[qv: 5b]] In addition, prenatal BPA exposure results in reduced spine number on the hippocampal CA1 areas of neonates African green monkeys and adult mice (14 month old). [[qv: 9a,27]] Even one injection of BPA (40 µg kg −1 ) can reduce dendritic spine density in the CA1 areas of adult male rats 22. Although exposure time, BPA dosage and experimental subjects of our study are different with those previous studies, the results are consistent with their morphological alterations.…”

Section: Discussionsupporting

confidence: 79%

“…According to previous reports, one week BPA exposure (40 µg kg −1 d −1 ) in adolescent rats impairs the object placement performance, which is also hippocampal‐dependent spatial memory 8. Moreover, acute BPA exposure in adult rats could cause the impairment of object placement memory 22. Our findings provide important “missing” evidence of BPA effects on hippocampal‐related function in the whole life of rats.…”

Section: Discussionsupporting

confidence: 74%

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Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Gong

et al. 2017

Advanced Science

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Bisphenol A (BPA), an environmental xenoestrogen, has been reported to induce learning and memory impairments in rodent animals. However, effects of BPA exposure on synaptic plasticity and the underlying physiological mechanisms remain elusive. Our behavioral and electrophysiological analyses show that BPA obviously perturbs hippocampal spatial memory of juvenile Sprague–Dawley rats after four weeks exposure, with significantly impaired long‐term potentiation (LTP) in the hippocampus. These effects involve decreased spine density of pyramidal neurons, especially the apical dendritic spine. Further presynaptic findings show an overt inhibition of pulse‐paired facilitation during electrophysiological recording, which suggest the decrease of presynaptic transmitter release and is consistent with reduced production of presynaptic glutamate after BPA exposure. Meanwhile, LTP‐related glutamate receptors, NMDA receptor 2A (NR2A) and AMPA receptor 1 (GluR1), are significantly downregulated in BPA‐exposed rats. Excitatory postsynaptic currents (EPSCs) results also show that EPSCNMDA, but not EPSCAMPA, is declined by 40% compared to the baseline in BPA‐perfused brain slices. Taken together, these findings reveal that juvenile BPA exposure has negative effects on synaptic plasticity, which result from decreases in dendritic spine density and excitatory synaptic transmission. Importantly, this study also provides new insights into the dynamics of BPA‐induced memory deterioration during the whole life of rats.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 74%

Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Gong

et al. 2017

Advanced Science

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“…PSD -95 is located in dendritic spines and is a key post-synaptic scaffold protein at excitatory synapses that directly promotes synapse maturation and exerts a major influence on synaptic strength and plasticity (40). Previous studies have shown that an increase in PSD -95 is correlated with enhanced hippocampal memory formation (16). Memory formation and neuronal adaptation also involve GAP-43 expressed in the hippocampus (41,42).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

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Background: Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. The purpose of this study was to investigate the effect of sevoflurane postconditioning on endogenous antioxidant status and spatial learning and memory ability after cardiac arrest (CA) and the potential underlying mechanisms. Methods: A rat model of CA was established by delivering an alternating current between the esophagus and chest wall to induce ventricular fibrillation. Animals were randomly divided into three groups: sham group (no CA), CA group, and CA + sevoflurane postconditioning (CA + SE) group. Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 60 min after resuscitation. The spatial learning and memory ability of rats was measured by the Morris water maze. The antioxidant enzymes activities were assessed at 4 hours, 1 day and 8 days after resuscitation. Moreover, the expressions of hippocampal proteins which could serve as memory enhancement biomarkers including growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD -95) and the transcription factor c-jun/activator protein-1 (AP-1), were detected at 8 days after resuscitation. Results: We found that CA significantly decreased the ability of spatial learning and memory in contrast to the sham controls. However, sevoflurane postconditioning significantly increased survival rate and antioxidant enzyme activities as well as ameliorated the spatial learning and memory deficits induced by CA. Furthermore, sevoflurane postconditioning regulated hippocampal memory enhancement proteins. Conclusions: Postconditioning with sevoflurane improved learning and memory deficits in a CA model possibly due to the reduction of oxidative stress and up-regulation of the memory enhancement biomarkers in hippocampus.

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“…Particularly, it is of interest that bisphenol A exerts a powerful impact on neural system [14][15][16]. It was shown using a dose that is below the USEPA reference safe daily limit of 50 µg/kg/day [31].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, in addition to developmental exposure to bisphenol A, there have been reported about exposure of adult animals to the chemical [14][15][16]. The current study was designed to examine whether exposure of adult rats to bisphenol A would cause neurodegeneration, particularly of dopaminergic neurons, resulting in a model of Parkinson's disease.…”

Section: Introductionmentioning

confidence: 99%

Temporal Effects of Bisphenol A on Dopaminergic Neurons: An Experiment on Adult Rats

Ishido

Masuo

2014

TOENVIRJ

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Abstract:The vulnerability of developing brains to environmental chemicals has been reported. Here, we examined the temporal effects of bisphenol A on dopaminergic neurons. Exposure of 5-day-old rats to bisphenol A caused hyperactivity in juveniles, after which spontaneous motor activity leveled off at 8 weeks of age, when apoptotic cell death was still observed along with the loss of tyrosine hydroxylase immunoreactivity. Accumulation of α-synuclein, a pathological marker of neurodegeneration, was also detectable in the substantia nigra, but not in the cerebral cortex. In adult rats, acute toxicity following microinjection of bisphenol A (20 µg) caused degeneration of dopaminergic neurons, similar to that following administration of 6-hydroxydopamine (15 µg). Chronic exposure of adult rats to bisphenol A (3 mg/kg/day for 28 days) caused neurodegeneration in the substantia nigra. However, behavioral effects were not seen after either acute or chronic exposure of adult rats to bisphenol A.Thus, the sensitivity of the central nervous system to bisphenol A was shown to be different at different life stages, confirming the greater vulnerability of the developing central nervous system.

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Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.

Cited by 107 publications

References 85 publications

Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Bisphenol A Impairs Synaptic Plasticity by Both Pre‐ and Postsynaptic Mechanisms

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Temporal Effects of Bisphenol A on Dopaminergic Neurons: An Experiment on Adult Rats

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