PREVIOUS studies have found an association between prior ethanol consu
mption and aggravated stroke outcome. Gerbils were intermittently give
n ethanol injections (s.c.) for 21 days at doses of 1 and 4 g/kg. Afte
r cessation of injections and appropriate weight gain, subjects underw
ent bilateral carotid occlusion while amino acid neurotransmitter leve
ls in the hippocampus were monitored. Both the low and high dose ethan
ol groups demonstrated significantly decreased glutamate release compa
red with saline-treated controls during ischemia (p < 0.05). These res
ults are consistent with a long-lasting ethanol-induced decrease in sy
naptic density in the hippocampus. That no intergroup differences on h
istological or neurobehavioral measures was found may suggest a functi
onal dissociation of glutaminergic involvement in the pathogenesis of
aggravated stroke outcome with alcoholism.