Food deprivation protects the rat striatum against hypoxia-ischemia despite high extracellular glutamate.
In a model that combines hypoxia with ischemia, the relationship between histological outcome, evoked rise in blood glucose, and striatal glutamate release was investigated in the 24-h food-deprived and normally fed rat. Food deprivation protected the dorsolateral striatum very effectively, as was shown with a silver stain. An online monitoring technique based on microdialysis showed that, in the protected condition, more glutamate was released into the striatal extracellular space than in the compromised condition. The possibility that the microdialysis results were influenced by a difference in shrinking of the extracellular space following food deprivation was excluded by the measurements of whole-tissue impedance. During the hypoxic-ischemic challenge, blood glucose rose in normally fed rats, but was suppressed almost completely after food deprivation. These results led us to conclude that, in our model of hypoxia-ischemia, the amount of glutamate released is not related directly to the extent of brain damage, but the increase in blood glucose may determine at least part of the brain damage.
Dijk
S N
SN
Department of Biological Psychiatry, University of Groningen, The Netherlands.
Krop-van Gastel
W
W
Obrenovitch
T P
TP
Korf
J
J
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004435:Eating; D005508:Food Deprivation; D005971:Glutamates / Q000378:metabolism / Q000502:physiology*; D018698:Glutamic Acid; D002534:Hypoxia, Brain / Q000503:physiopathology* / Q000517:prevention & control; D002546:Ischemic Attack, Transient / Q000503:physiopathology* / Q000517:prevention & control; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D001786:Blood Glucose; D005971:Glutamates; D018698:Glutamic Acid