Sex-specific effects of bisphenol-A on memory and synaptic structural modification in hippocampus of adult mice

Xu, Xiaoling; Liu, Xingyi; Zhang, Qin; Zhang, Guangxia; Lu, Yingjun; Ruan, Qiurong; Fang, Dong; Yang, Yanling

doi:10.1016/j.yhbeh.2013.03.004

Cited by 57 publications

(55 citation statements)

References 65 publications

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“…Accepting these shortcomings, the area of a PC–PC contact was calculated to be approximately 50% larger in CB–/– terminals. Studies that reported on the width of the synaptic cleft found the cleft width to show extremely little variation (SD in the order of <5%) for a given synapse type (Jing et al, 2004; Xu and Zhang, 2006; Xu et al, 2013a,b; Han et al, 2014). Changes in cleft width are most often the result of experimental manipulations including OGD, “metal-poisoning” by lead and aluminum (Jing et al, 2004; Lushnikova et al, 2011; Han et al, 2014), but were also observed in genetic models, e.g., CNTNAP4-KO mice (Karayannis et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…After 60 min OGD, AZ area increased by 58% (Lushnikova et al, 2011) and also the volume of the presynaptic terminal was augmented. In the other models, where cleft width was increased, the length of the AZ was either unaltered, as in the case of estradiol benzoate treatment (Xu et al, 2006) or even reduced as in the cases of bisphenol-A-mediated inhibition of synaptogenesis (Xu et al, 2013a,b) and exposure to either lead (Han et al, 2014) or aluminum (Jing et al, 2004). …”

Section: Discussionmentioning

confidence: 99%

“…Structural changes with respect to synaptic cleft width, dimension of the AZ/PSD, curvature and presynaptic bouton volume have been reported. These changes are often the result of short- or long-term pathological insults such as oxygen/glucose deprivation (OGD; Lushnikova et al, 2011), long-term exposure to lead (Han et al, 2014), aluminum (Jing et al, 2004) or biphenyl-A, a presumed endocrine disruptor (Xu et al, 2013a,b). But also exposure of ovarectomized (OVX) rats to estradiol benzoate increases the synaptic cleft width of CA1 hippocampal synapses in the pyramidal cell layer (Xu and Zhang, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Subcellular structural plasticity caused by the absence of the fast Ca2+ buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons

Orduz

Boom

Gall

et al. 2014

Front. Cell. Neurosci.

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Purkinje cells (PC) control spike timing of neighboring PC by their recurrent axon collaterals. These synapses underlie fast cerebellar oscillations and are characterized by a strong facilitation within a time window of <20 ms during paired-pulse protocols. PC express high levels of the fast Ca2+ buffer protein calbindin D-28k (CB). As expected from the absence of a fast Ca2+ buffer, presynaptic action potential-evoked [Ca2+]i transients were previously shown to be bigger in PC boutons of young (second postnatal week) CB-/- mice, yet IPSC mean amplitudes remained unaltered in connected CB–/– PC. Since PC spine morphology is altered in adult CB–/– mice (longer necks, larger spine head volume), we summoned that morphological compensation/adaptation mechanisms might also be induced in CB–/– PC axon collaterals including boutons. In these mice, biocytin-filled PC reconstructions revealed that the number of axonal varicosities per PC axon collateral was augmented, mostly confined to the granule cell layer. Additionally, the volume of individual boutons was increased, evidenced from z-stacks of confocal images. EM analysis of PC–PC synapses revealed an enhancement in active zone (AZ) length by approximately 23%, paralleled by a higher number of docked vesicles per AZ in CB–/– boutons. Moreover, synaptic cleft width was larger in CB–/– (23.8 ± 0.43 nm) compared to wild type (21.17 ± 0.39 nm) synapses. We propose that the morphological changes, i.e., the larger bouton volume, the enhanced AZ length and the higher number of docked vesicles, in combination with the increase in synaptic cleft width likely modifies the GABA release properties at this synapse in CB–/– mice. We view these changes as adaptation/homeostatic mechanisms to likely maintain characteristics of synaptic transmission in the absence of the fast Ca2+ buffer CB. Our study provides further evidence on the functioning of the Ca2+ homeostasome.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Subcellular structural plasticity caused by the absence of the fast Ca2+ buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons

Orduz

Boom

Gall

et al. 2014

Front. Cell. Neurosci.

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“…Two other papers by the same group reported a decreased expression of NMDA and AMPA receptors in mice hippocampus using a transgenerational protocol of BPA administration (400-40000 µg/Kg/day) inhibiting synaptogenesis and sex-specific effects in memory and synaptic structure [50,51]. It is remarkable that most of the effects of BPA on ionotropic glutamate receptors by Xu and coworkers were observed at doses relevant to human exposure.…”

Section: Ionotropic Glutamate Receptorsmentioning

confidence: 97%

Effects of Bisphenol A on ion channels: Experimental evidence and molecular mechanisms

et al. 2016

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Please cite this article as: Soriano, S., Ripoll, C., Alonso-Magdalena, P., Fuentes, E., Quesada, I., Nadal, A., Martinez-Pinna, J., Effects of Bisphenol A on ion channels: experimental evidence and molecular mechanisms, Steroids (2016), doi: http://dx.doi.org/10. 1016/j.steroids.2016.02.020 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Various studies have reported that BPA affects glutamate receptors (NMDARs and AMPARs) and produces neurotoxicity (Xu X. et al, 2010; Xu X.H. et al, 2010; Xu X. et al, 2013). According to a recent study, GluN2A and GluA1 (LTP-related glutamate receptors) were significantly downregulated in BPA-exposed rats (Hu F. et al, 2017).…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

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Glutamate receptors play a crucial role in the central nervous system and are implicated in different brain disorders. They play a significant role in the pathogenesis of neurodegenerative diseases (NDDs) such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Although many studies on NDDs have been conducted, their exact pathophysiological characteristics are still not fully understood. In in vivo and in vitro models of neurotoxic-induced NDDs, neurotoxic agents are used to induce several neuronal injuries for the purpose of correlating them with the pathological characteristics of NDDs. Moreover, therapeutic drugs might be discovered based on the studies employing these models. In NDD models, different neurotoxic agents, namely, kainic acid, domoic acid, glutamate, β-N-Methylamino-L-alanine, amyloid beta, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenylpyridinium, rotenone, 3-Nitropropionic acid and methamphetamine can potently impair both ionotropic and metabotropic glutamate receptors, leading to the progression of toxicity. Many other neurotoxic agents mainly affect the functions of ionotropic glutamate receptors. We discuss particular neurotoxic agents that can act upon glutamate receptors so as to effectively mimic NDDs. The correlation of neurotoxic agent-induced disease characteristics with glutamate receptors would aid the discovery and development of therapeutic drugs for NDDs.

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Sex-specific effects of bisphenol-A on memory and synaptic structural modification in hippocampus of adult mice

Cited by 57 publications

References 65 publications

Subcellular structural plasticity caused by the absence of the fast Ca2+ buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons

Subcellular structural plasticity caused by the absence of the fast Ca2+ buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons

Effects of Bisphenol A on ion channels: Experimental evidence and molecular mechanisms

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

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