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Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes
Alternative TitleArsenic exposure and glutamate-induced gliotransmitter release from astrocytes ☆
Wang Yan1; Zhao Fenghong1; Liao Yingjun2; Jin Yaping1; Sun Guifan1
2012
Source PublicationNEURAL REGENERATION RESEARCH
ISSN1673-5374
Volume7Issue:31Pages:2439-2445
AbstractThe present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 mu M arsenite for 24 hours. Cell viability and morphological observations revealed that 5 mu M arsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 mu M arsenite for 24 hours and stimulated with 25 mu M glutamate for 10 minutes. Results showed that Ca2+(i) in astrocytes exposed to 5 and 10 mu M arsenite was significantly increased and levels of D-serine, y-aminobutyric acid and glycine in cultures exposed to 2.5-10 mu M arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 mu M arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function.
Other AbstractThe present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 μM arsenite for 24 hours. Cell viability and morphological observations revealed that 5 μM arsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 μM arsenite for 24 hours and stimulated with 25 μM glutamate for 10 minutes. Results showed that Ca 2+ i in astrocytes exposed to 5 and 10 μM arsenite was significantly increased and levels of D-serine, γ-aminobutyric acid and glycine in cultures exposed to 2.5–10 μM arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 μM arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function.
KeywordINTELLECTUAL FUNCTION NEURONAL-ACTIVITY DRINKING-WATER GLIAL-CELLS D-SERINE MODULATION RELEVANCE CHILDREN COMMUNICATION BANGLADESH arsenite astrocyte glutamate neuron cell viability intracellular free calcium gliotransmitter neurotoxicity neural regeneration
Indexed ByCSCD
Language英语
Funding Project[National Natural Science Foundation of China]
CSCD IDCSCD:4694373
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Document Type期刊论文
Identifierhttp://ir.imr.ac.cn/handle/321006/156051
Collection中国科学院金属研究所
Affiliation1.中国科学院金属研究所
2.华东师范大学
Recommended Citation
GB/T 7714
Wang Yan,Zhao Fenghong,Liao Yingjun,et al. Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes[J]. NEURAL REGENERATION RESEARCH,2012,7(31):2439-2445.
APA Wang Yan,Zhao Fenghong,Liao Yingjun,Jin Yaping,&Sun Guifan.(2012).Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes.NEURAL REGENERATION RESEARCH,7(31),2439-2445.
MLA Wang Yan,et al."Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes".NEURAL REGENERATION RESEARCH 7.31(2012):2439-2445.
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