ABSTRACT
Ethanol (1 g/kg, orally) disturbed the hole reflex in male SHR and C57BL/6 mice and common albino rats increasing the time spent in the light part of a dark-light chamber. In mice this effect was often accompanied by an increase in number of transitions between dark and light compartments. Intraperitoneal pretreatment with endogenous metabolites of tryptophan in the kynurenine pathway of its metabolism (kynurenines)--kynurenic, picolinic and xanthurenic acids--attenuated the effect of ethanol in mice. Injection into the brain ventricles of the most active kynurenines from the group of excitatory amino acids, quinolinic acid and its precursor kynurenine, counteracted ethanol in mice and rats. The same was true in mice for intracerebroventricularly administered kynurenic, picolinic and xanthurenic acids.
