Effect of acute alcohol on ischemia-induced glutamate release and brain damage.
Epidemiological studies show that chronic ethanol consumption at high doses enhances the risk of cerebral stroke. The mechanisms responsible for the greater vulnerability of alcoholics' brains to stroke have to be completely understood, but a role for excitatory amino acids has been suggested. In order to study the interaction between alcohol and ischemia, we investigated the effect of acute alcohol administration in a model of focal cerebral ischemia. In particular, we evaluated the release of glutamate and aspartate from the cerebral frontal cortex by a transdialysis technique. Alcohol was acutely administered at 1.5 and 3.0 g/kg ip. During the period of maximal alcoholemia, ethanol almost abolished the ischemia-induced release of glutamate leading to glutamate values around or below the basal. Aspartate levels were unaltered both following ischemia and alcohol+ischemia. The decrease in glutamate release, however, was not accompanied by a significant reduction of the extension of the damaged area assessed by histological analysis.
Masoero
E
E
Department of Experimental and Applied Pharmacology, University of Pavia, Viale Taramelli 14, 27100 Pavia, Italy.
Frattini
P
P
Favalli
L
L
Rozza
A
A
Scelsi
R
R
Govoni
S
S
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001921:Brain / Q000473:pathology; D001927:Brain Diseases / Q000209:etiology* / Q000473:pathology; D002545:Brain Ischemia / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D000431:Ethanol / Q000008:administration & dosage* / Q000097:blood / Q000494:pharmacology; D005625:Frontal Lobe / Q000187:drug effects / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009336:Necrosis; D051381:Rats; D017208:Rats, Wistar; D012395:Rose Bengal / Q000494:pharmacology
D012395:Rose Bengal; D001224:Aspartic Acid; D000431:Ethanol; D018698:Glutamic Acid