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Perinatal exposure to bisphenol-A impairs spatial memory through upregulation of neurexin1 and neuroligin3 expression in male mouse brain.

Kumar D, Thakur MK - PLoS ONE (2014)

Bottom Line: RT-PCR and Immunoblotting results showed significant upregulation of Nrxn1 and Nlgn3 expression in both cerebral cortex and hippocampus of 3 and 8 weeks male mice.This was further substantiated by in-situ hybridization and immunofluorescence techniques.BPA also significantly increased the density of dendritic spines in both regions, as analyzed by rapid Golgi staining.

View Article: PubMed Central - PubMed

Affiliation: Biochemistry and Molecular Biology Laboratory, Brain Research Centre, Department of Zoology, Banaras Hindu University, Varanasi, India.

ABSTRACT
Bisphenol-A (BPA), a well known endocrine disruptor, impairs learning and memory in rodents. However, the underlying molecular mechanism of BPA induced impairment in learning and memory is not well known. As synaptic plasticity is the cellular basis of memory, the present study investigated the effect of perinatal exposure to BPA on the expression of synaptic proteins neurexin1 (Nrxn1) and neuroligin3 (Nlgn3), dendritic spine density and spatial memory in postnatal male mice. The pregnant mice were orally administered BPA (50 µg/kgbw/d) from gestation day (GD) 7 to postnatal day (PND) 21 and sesame oil was used as a vehicle control. In Morris water maze (MWM) test, BPA extended the escape latency time to locate the hidden platform in 8 weeks male mice. RT-PCR and Immunoblotting results showed significant upregulation of Nrxn1 and Nlgn3 expression in both cerebral cortex and hippocampus of 3 and 8 weeks male mice. This was further substantiated by in-situ hybridization and immunofluorescence techniques. BPA also significantly increased the density of dendritic spines in both regions, as analyzed by rapid Golgi staining. Thus our data suggest that perinatal exposure to BPA impairs spatial memory through upregulation of expression of synaptic proteins Nrxn1 and Nlgn3 and increased dendritic spine density in cerebral cortex and hippocampus of postnatal male mice.

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Effect of perinatal exposure to BPA on dendritic spine density in cerebral cortex and hippocampus of male mice.Rapid Golgi staining of neurons in the cerebral cortex and hippocampus of 3 and 8 weeks male mice. The histograms represent the number of dendritic spines/10 µm length of primary dendrites. Each bar represents the mean ± SEM of 15 neurons from three independent experiments and * denotes the significant difference (p<0.05) between sesame oil and BPA exposed mice.
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pone-0110482-g006: Effect of perinatal exposure to BPA on dendritic spine density in cerebral cortex and hippocampus of male mice.Rapid Golgi staining of neurons in the cerebral cortex and hippocampus of 3 and 8 weeks male mice. The histograms represent the number of dendritic spines/10 µm length of primary dendrites. Each bar represents the mean ± SEM of 15 neurons from three independent experiments and * denotes the significant difference (p<0.05) between sesame oil and BPA exposed mice.

Mentions: The rapid Golgi stain impregnation clearly filled the basilar dendritic shaft and spines of cortical and hippocampal neurons in 3 and 8 weeks male mice. The dendritic spine density was significantly higher in BPA exposed group as compared to control (Fig. 6A, B) in the cerebral cortex (p<0.01) and hippocampus (p<0.01) of both 3 and 8 weeks male mice. However, the effect of perinatal exposure to BPA was higher in hippocampus as compared to cerebral cortex. The increased number of dendritic spines persisted even after the BPA exposure was stopped.


Perinatal exposure to bisphenol-A impairs spatial memory through upregulation of neurexin1 and neuroligin3 expression in male mouse brain.

Kumar D, Thakur MK - PLoS ONE (2014)

Effect of perinatal exposure to BPA on dendritic spine density in cerebral cortex and hippocampus of male mice.Rapid Golgi staining of neurons in the cerebral cortex and hippocampus of 3 and 8 weeks male mice. The histograms represent the number of dendritic spines/10 µm length of primary dendrites. Each bar represents the mean ± SEM of 15 neurons from three independent experiments and * denotes the significant difference (p<0.05) between sesame oil and BPA exposed mice.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4201550&req=5

pone-0110482-g006: Effect of perinatal exposure to BPA on dendritic spine density in cerebral cortex and hippocampus of male mice.Rapid Golgi staining of neurons in the cerebral cortex and hippocampus of 3 and 8 weeks male mice. The histograms represent the number of dendritic spines/10 µm length of primary dendrites. Each bar represents the mean ± SEM of 15 neurons from three independent experiments and * denotes the significant difference (p<0.05) between sesame oil and BPA exposed mice.
Mentions: The rapid Golgi stain impregnation clearly filled the basilar dendritic shaft and spines of cortical and hippocampal neurons in 3 and 8 weeks male mice. The dendritic spine density was significantly higher in BPA exposed group as compared to control (Fig. 6A, B) in the cerebral cortex (p<0.01) and hippocampus (p<0.01) of both 3 and 8 weeks male mice. However, the effect of perinatal exposure to BPA was higher in hippocampus as compared to cerebral cortex. The increased number of dendritic spines persisted even after the BPA exposure was stopped.

Bottom Line: RT-PCR and Immunoblotting results showed significant upregulation of Nrxn1 and Nlgn3 expression in both cerebral cortex and hippocampus of 3 and 8 weeks male mice.This was further substantiated by in-situ hybridization and immunofluorescence techniques.BPA also significantly increased the density of dendritic spines in both regions, as analyzed by rapid Golgi staining.

View Article: PubMed Central - PubMed

Affiliation: Biochemistry and Molecular Biology Laboratory, Brain Research Centre, Department of Zoology, Banaras Hindu University, Varanasi, India.

ABSTRACT
Bisphenol-A (BPA), a well known endocrine disruptor, impairs learning and memory in rodents. However, the underlying molecular mechanism of BPA induced impairment in learning and memory is not well known. As synaptic plasticity is the cellular basis of memory, the present study investigated the effect of perinatal exposure to BPA on the expression of synaptic proteins neurexin1 (Nrxn1) and neuroligin3 (Nlgn3), dendritic spine density and spatial memory in postnatal male mice. The pregnant mice were orally administered BPA (50 µg/kgbw/d) from gestation day (GD) 7 to postnatal day (PND) 21 and sesame oil was used as a vehicle control. In Morris water maze (MWM) test, BPA extended the escape latency time to locate the hidden platform in 8 weeks male mice. RT-PCR and Immunoblotting results showed significant upregulation of Nrxn1 and Nlgn3 expression in both cerebral cortex and hippocampus of 3 and 8 weeks male mice. This was further substantiated by in-situ hybridization and immunofluorescence techniques. BPA also significantly increased the density of dendritic spines in both regions, as analyzed by rapid Golgi staining. Thus our data suggest that perinatal exposure to BPA impairs spatial memory through upregulation of expression of synaptic proteins Nrxn1 and Nlgn3 and increased dendritic spine density in cerebral cortex and hippocampus of postnatal male mice.

Show MeSH
Related in: MedlinePlus