Ischemic neuronal damage. How does mild hypothermia modulate it?
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.
Kataoka
K
K
Department of Physiology, Ehime University School of Medicine, Japan.
Mitani
A
A
Yanase
H
H
Zhang
L
L
Higashihara
M
M
Ogata
T
T
Tsuji
K
K
Nakamura
Y
Y
McRae
A
A
Ogita
K
K
Yoneda
Y
Y
D000818:Animals; D001921:Brain / Q000473:pathology / Q000502:physiology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy*; D004247:DNA / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007036:Hypothermia, Induced; D009474:Neurons / Q000473:pathology* / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D018808:Transcription Factor AP-1 / Q000378:metabolism
D004268:DNA-Binding Proteins; D016194:Receptors, N-Methyl-D-Aspartate; D018808:Transcription Factor AP-1; D018698:Glutamic Acid; D004247:DNA