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Food Deprivation Protects the Rat Striatum Against Hypoxia‐Ischemia Despite High Extracellular Glutamate
Author(s) -
Dijk S. N.,
Gastel W. Kropvan,
Obrenovitch T. P.,
Korf J.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62051847.x
Subject(s) - microdialysis , glutamate receptor , striatum , hypoxia (environmental) , extracellular , ischemia , extracellular fluid , endocrinology , medicine , neuroscience , chemistry , biology , biochemistry , dopamine , receptor , organic chemistry , oxygen
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 on‐ line monitoring technique based on microdialysis showed that, in the protected condition, more glutamate was re‐ leased into the striatal extracellular space than in the com‐ promised condition. The possibility that the microdialysis results were influenced by a difference in shrinking of the extracellular space following food deprivation was ex‐ cluded by the measurements of whole‐tissue impedance. During the hypoxic‐ischemic challenge, blood glucose rose in normally fed rats, but was suppressed almost com‐ pletely after food deprivation. These results led us to con‐ clude 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.