Skip to main content
Log in

Ischemic neuronal damage

How does mild hypothermia modulate it?

  • Part VIII Therapeutic Strategies
  • Published:
Molecular and chemical neuropathology

Abstract

The significance of mild hypothermia as a therapeutic measure for ischemic brain damage is presented on the basis of different experimental results. An extracellular glutamate surge, a sustained activation of N-methyl-D-aspartate (NMDA) receptors, and an enhancement of DNA binding activity to transcription factor AP-1, all being key items directly linked to excitotoxic neuronal damage, are deeply affected by slightly lowering temperature (mild hypothermia [MH]). The cellular mechanism of MH seems rather nonspecific but tends to collectively involve these key items rendering neurons resistant to ischemic damage. Clinical application of MH should be a great challenge to relieve deadly effects on central neurons.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  • Fay T. (1940) Observations on prolonged human refrigeration.NY State J. Med. 40, 1351–1354.

    Google Scholar 

  • Kirino T. (1982) Delayed neuronal death in the gerbil hippocampus following ischemia.Brain Res. 239, 57–69.

    Article  CAS  Google Scholar 

  • Mitani A. and Kataoka K. (1991) Critical levels of extracellular glutamate mediating gerbil hippocampal delayed neuronal death during hypothermia: Brain microdialysis study.Neuroscience 42, 661–670.

    Article  CAS  Google Scholar 

  • Mitani A., Andou Y., Matsuda S., Arai T., Sakanaka M., and Kataoka K. (1994) Origin of ischemia-induced glutamate efflux in field CA1 of the gerbil hippocampus: An in vivo brain microdialysis study.J. Neurochem. 63, 2152–2164.

    Article  CAS  Google Scholar 

  • Ogata T., Nakamura Y., Shibata T., and Kataoka K. (1992) Release of excitatory amino acids from cultured hippocampal astrocytes induced by a hypoxichypoglycemic stimulation.J. Neurochem. 58, 1957–1959.

    Article  CAS  Google Scholar 

  • Pulsinelli W. A., Brierley J. B., and Plum F. (1982) Temporal profile of neuronal damage in a model of transient forebrain ischemia.Ann. Neurol. 11, 491–498.

    Article  CAS  Google Scholar 

  • Rothman S. M. and Olney J. W. (1986) Glutamate and the pathophysiology of hypoxic-ischemic brain damage.Ann. Neurol. 19, 105–111.

    Article  CAS  Google Scholar 

  • Shimada N., Graf R., Rosner G., Wakayama A., George C. P., and Heiss W.-D. (1989) Ischemic flow threshold for extracellular glutamate increase in cat cortex.J. Cereb. Blood Flow Met. 9, 603–606.

    Article  CAS  Google Scholar 

  • Yoneda Y., Ogita K., Inoue K., Mitani A., Zhang L., Masuda S., Higashihara M., and Kataoka K. (1994) Rapid potentiation of DNA binding activities of particular transcription factors with leucine-zipper motifs in discrete brain structures of the gerbil with transient forebrain ischemia.Brain Res. 667, 54–66.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Kataoka, K., Mitani, A., Yanase, H. et al. Ischemic neuronal damage. Molecular and Chemical Neuropathology 28, 191–195 (1996). https://doi.org/10.1007/BF02815222

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF02815222

Index Entries

Navigation