Involvement of Glutamate transporter-1 in neuroprotection against global brain ischemia-reperfusion injury induced by postconditioning in rats

Int J Mol Sci. 2010 Nov 3;11(11):4407-16. doi: 10.3390/ijms11114407.

Abstract

Ischemic postconditioning refers to several transient reperfusion and ischemia cycles after an ischemic event and before a long duration of reperfusion. The procedure produces neuroprotective effects. The mechanisms underlying these neuroprotective effects are poorly understood. In this study, we found that most neurons in the CA1 region died after 10 minutes of ischemia and is followed by 72 hours of reperfusion. However, brain ischemic postconditioning (six cycles of 10 s/10 s reperfusion/re-occlusion) significantly reduced neuronal death. Significant up-regulation of Glutamate transporter-1 was found after 3, 6, 24, 72 hours of reperfusion. The present study showed that ischemic postconditioning decreases cell death and that upregulation of GLT-1 expression may play an important role on this effect.

Keywords: brain ischemia reperfusion injury; glutamate transporter 1(GLT-1); ischemic postconditioning; neuroprotection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CA1 Region, Hippocampal / blood supply
  • CA1 Region, Hippocampal / metabolism*
  • CA1 Region, Hippocampal / pathology
  • Cell Death
  • Excitatory Amino Acid Transporter 2 / genetics
  • Excitatory Amino Acid Transporter 2 / metabolism*
  • Ischemic Postconditioning*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / therapy

Substances

  • Excitatory Amino Acid Transporter 2
  • Slc1a2 protein, rat