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Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models

  • Authors:
    • Zhongrun Qian
    • Yingying Lin
    • Jin Xing
    • Yongming Qiu
    • Li Ren
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China, Department of Neurosurgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai 201399, P.R. China
    Copyright: © Qian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 8196-8202
    |
    Published online on: April 16, 2018
       https://doi.org/10.3892/mmr.2018.8888
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Abstract

Glutamate and γ‑aminobutyric acid (GABA) transporters serve central roles in normal neuronal activity and are associated with numerous pathological brain conditions, including ischemia and epilepsy. However, the interplay between these transporters in ischemia remains unclear. In the present study, the expression levels of the excitatory amino acid carrier 1 (EAAC1) and GABA transporter 1 (GAT1) were analyzed in vivo and in vitro within ischemic models by immunofluorescence, western blot and RT‑qPCR. Cell survival rates were analyzed following altered expression of these transporters within neuronal cells by flow cytometry. Expression levels of EAAC1 were reduced within the cerebrum of focal cerebral ischemic middle cerebral artery occlusion rat models as well as in primary neurons cultured under hypoxia. However, GAT1 expression levels were slightly elevated under ischemic conditions. The altered expression levels of EAAC1 and GAT1 were combined within neuron cells and the effects were investigated. Apoptotic analysis revealed that EAAC1 suppression and overexpression of GAT1 increased neuronal cell apoptosis under hypoxic conditions; however, EAAC1 overexpression combined with GAT1 knockdown reduced neuronal cell apoptosis under hypoxic conditions. The present study detected the expression levels of the glutamate and GABA transporters under hypoxia, in association with ischemia. The results indicated that, increased expression of EAAC1 combined with GAT1 suppression may provide protective effects in the treatment of epilepsy and ischemia.
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Copy and paste a formatted citation
Spandidos Publications style
Qian Z, Lin Y, Xing J, Qiu Y and Ren L: Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models. Mol Med Rep 17: 8196-8202, 2018.
APA
Qian, Z., Lin, Y., Xing, J., Qiu, Y., & Ren, L. (2018). Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models. Molecular Medicine Reports, 17, 8196-8202. https://doi.org/10.3892/mmr.2018.8888
MLA
Qian, Z., Lin, Y., Xing, J., Qiu, Y., Ren, L."Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models". Molecular Medicine Reports 17.6 (2018): 8196-8202.
Chicago
Qian, Z., Lin, Y., Xing, J., Qiu, Y., Ren, L."Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models". Molecular Medicine Reports 17, no. 6 (2018): 8196-8202. https://doi.org/10.3892/mmr.2018.8888
Copy and paste a formatted citation
x
Spandidos Publications style
Qian Z, Lin Y, Xing J, Qiu Y and Ren L: Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models. Mol Med Rep 17: 8196-8202, 2018.
APA
Qian, Z., Lin, Y., Xing, J., Qiu, Y., & Ren, L. (2018). Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models. Molecular Medicine Reports, 17, 8196-8202. https://doi.org/10.3892/mmr.2018.8888
MLA
Qian, Z., Lin, Y., Xing, J., Qiu, Y., Ren, L."Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models". Molecular Medicine Reports 17.6 (2018): 8196-8202.
Chicago
Qian, Z., Lin, Y., Xing, J., Qiu, Y., Ren, L."Expression and functions of glutamate and γ‑aminobutyric acid transporters in ischemic models". Molecular Medicine Reports 17, no. 6 (2018): 8196-8202. https://doi.org/10.3892/mmr.2018.8888
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