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Glial metabolic dysfunction caused neural damage by short-term ischemia in brain

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Abstract

Although several pieces of evidence have indicated that glial cells support neuronal cells in the ischemia-reperfusion brain, the direct contribution of glial cells to cell damage is not well known. The present study was designed to determine whether there are any changes in cell damage after a short-term middle cerebral artery occlusion (MCAO) when glial metabolism is suppressed. Injection of fluorocitrate (FC) or 10 minutes MCAO alone did not produce cell damage. However, 10 minutes MCAO in rats pretreated with FC caused significant cell damage. These data directly demonstrated that inhibition of glial metabolism might increase neuronal vulnerability to even a short-term transient ischemia.

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Authors and Affiliations

  1. Course of Allied Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita, 565-0871, Osaka, Japan

    Rie Hosoi, Yuto Kashiwagi & Osamu Inoue

  2. Department of Nuclear Medicine and Tracer Kinetics, Osaka University Graduate School of Medicine, Osaka, Japan

    Jun Hatazawa

  3. GlaxoSmithkline, Clinical Research Unit, ACCl, Cambridge, UK

    Antony Gee

Authors
  1. Rie Hosoi
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  2. Yuto Kashiwagi
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  3. Jun Hatazawa
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  4. Antony Gee
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  5. Osamu Inoue
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Correspondence to Rie Hosoi.

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Hosoi, R., Kashiwagi, Y., Hatazawa, J. et al. Glial metabolic dysfunction caused neural damage by short-term ischemia in brain. Ann Nucl Med 20, 377–380 (2006). https://doi.org/10.1007/BF02987251

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  • DOI: https://doi.org/10.1007/BF02987251

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