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Journal of Molecular Neuroscience

, Volume 49, Issue 1, pp 21–27 | Cite as

Trichostatin A Enhances Glutamate Transporter GLT-1 mRNA Levels in C6 Glioma Cells via Neurosteroid-Mediated Cell Differentiation

  • Mari Itoh
  • Takara Hiroi
  • Naoyoshi Nishibori
  • Takefumi Sagara
  • Song Her
  • Mi-Sook Lee
  • Kyoji MoritaEmail author
Article

Abstract

The neurotoxic effects of excitatory amino acids (EAAs) are suggested to be connected with the chronic loss of neuronal cells, thereby being responsible for the age-related neurodegenerative diseases. Therefore, it seems conceivable that the excitatory amino acid transporters may contribute to the protection of neuronal cells against the excitotoxic damage by facilitating the removal of EAAs from the brain tissue. On the other hand, previous studies have suggested that glial cell differentiation may be involved in the protection and recovery of neural function probably through the elevation of BDNF gene expression in the brain. Based on these findings, histone deacetylase (HDAC) inhibitors are assumed to induce glutamate transporter-1 (GLT-1) gene expression probably through the promotion of glial cell differentiation. Then, we examined the effects of HDAC inhibitors on GLT-1 mRNA levels in rat C6 glioma cells and found that trichostatin A can induce GLT-1 gene transcription following steroid 5α-reductase and GFAP gene expression. Therefore, it seems conceivable that glial cell differentiation may play a potential role in the removal of EAAs probably through the expression of GLT-1, thereby being involved in the protection of neuronal cells against the chronic excitotoxic insults in the brain.

Keywords

Trichostatin A Glial cell differentiation GLT-1 gene expression Neuroprotective function Excitotoxic damage 

Notes

Acknowledgments

This work was supported in part by the funds provided by Kohken Co. Inc. (Sapporo, Japan) and Navio Co. Ltd. (Hiroshima, Japan).

Conflict of Interest Statement

There is no conflict of interest associated with the authors of this paper, and the fund sponsors did not cause any inappropriate influence on this work.

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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Mari Itoh
    • 1
  • Takara Hiroi
    • 1
  • Naoyoshi Nishibori
    • 2
  • Takefumi Sagara
    • 2
  • Song Her
    • 3
  • Mi-Sook Lee
    • 3
  • Kyoji Morita
    • 1
    Email author
  1. 1.Laboratory of Neuropharmacology, Department of NursingShikoku University School of Health SciencesTokushimaJapan
  2. 2.Laboratory of Cell Biology and Toxicology, Department of Food Science and NutritionShikoku Junior CollegeTokushimaJapan
  3. 3.Division of Bio-Imaging, Chuncheon CenterKorea Basic Science InstituteChuncheonSouth Korea

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