Open Access

Ischemic preconditioning protects neurons from damage and maintains the immunoreactivity of kynurenic acid in the gerbil hippocampal CA1 region following transient cerebral ischemia

  • Authors:
    • Jae-Chul Lee
    • Hyun-Jin Tae
    • Geum-Sil Cho
    • In Hye Kim
    • Ji Hyeon Ahn
    • Joon Ha Park
    • Bai Hui Chen
    • Jeong-Hwi Cho
    • Bich Na Shin
    • Jun Hwi Cho
    • Eun Joo Bae
    • Jinseu Park
    • Young-Myeong Kim
    • Soo Young Choi
    • Moo-Ho Won
  • View Affiliations

  • Published online on: April 7, 2015     https://doi.org/10.3892/ijmm.2015.2171
  • Pages: 1537-1544
  • Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Pyramidal neurons in region I of hippocampus proper (CA1) are particularly vulnerable to excitotoxic processes following transient forebrain ischemia. Kynurenic acid (KYNA) is a small molecule derived from tryptophan when this amino acid is metabolized through the kynurenine pathway. In the present study, we examined the effects of ischemic preconditioning (IPC) on the immunoreactivity and protein levels of KYNA following 5 min of transient forebrain ischemia in gerbils. The animals were randomly assigned to 4 groups (sham-operated group, ischemia-operated group, IPC + sham-operated group and IPC + ischemia-operated group). IPC was induced by subjecting the gerbils to 2 min of ischemia followed by 1 day of recovery. In the ischemia-operated group, we observed a significant loss of pyramidal neurons in the CA1 stratum pyramidale (SP) at 5 days post-ischemia; however, in the IPC + ischemia-operated group, the pyramidal neurons were well protected. KYNA immunoreactivity in the SP of the ischemia-operated group was significantly altered following ischemia-reperfusion and was very low 5 days following ischemia‑reperfusion. In the IPC + ischemia-operated group, however, KYNA immunoreactivity was constitutively detected in the SP of the CA1 region after the ischemic insult. We also found that the alteration pattern of the KYNA protein level in the CA1 region following ischemia was generally similar to the immunohistochemical changes observed. In brief, our findings demonstrated that IPC maintained and even increased KYNA immunoreactivity in the SP of the CA1 region following ischemia‑reperfusion. The data from the present study thus indicate that the enhancement of KYNA expression by IPC may be necessary for neuronal survival following transient ischemic injury.
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June-2015
Volume 35 Issue 6

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Lee J, Tae H, Cho G, Kim IH, Ahn JH, Park JH, Chen BH, Cho J, Shin BN, Cho JH, Cho JH, et al: Ischemic preconditioning protects neurons from damage and maintains the immunoreactivity of kynurenic acid in the gerbil hippocampal CA1 region following transient cerebral ischemia. Int J Mol Med 35: 1537-1544, 2015
APA
Lee, J., Tae, H., Cho, G., Kim, I.H., Ahn, J.H., Park, J.H. ... Won, M. (2015). Ischemic preconditioning protects neurons from damage and maintains the immunoreactivity of kynurenic acid in the gerbil hippocampal CA1 region following transient cerebral ischemia. International Journal of Molecular Medicine, 35, 1537-1544. https://doi.org/10.3892/ijmm.2015.2171
MLA
Lee, J., Tae, H., Cho, G., Kim, I. H., Ahn, J. H., Park, J. H., Chen, B. H., Cho, J., Shin, B. N., Cho, J. H., Bae, E. J., Park, J., Kim, Y., Choi, S. Y., Won, M."Ischemic preconditioning protects neurons from damage and maintains the immunoreactivity of kynurenic acid in the gerbil hippocampal CA1 region following transient cerebral ischemia". International Journal of Molecular Medicine 35.6 (2015): 1537-1544.
Chicago
Lee, J., Tae, H., Cho, G., Kim, I. H., Ahn, J. H., Park, J. H., Chen, B. H., Cho, J., Shin, B. N., Cho, J. H., Bae, E. J., Park, J., Kim, Y., Choi, S. Y., Won, M."Ischemic preconditioning protects neurons from damage and maintains the immunoreactivity of kynurenic acid in the gerbil hippocampal CA1 region following transient cerebral ischemia". International Journal of Molecular Medicine 35, no. 6 (2015): 1537-1544. https://doi.org/10.3892/ijmm.2015.2171