Brain catalase mediates potentiation of social recognition memory produced by ethanol in mice

The involvement of catalase in ethanol-induced locomotion has been clearly proven. However, studies addressing the role of this enzyme in the effects that ethanol exerts on memory are lacking. In the present study, the social recognition test (SRT) was used to evaluate ethanol effects on memory. In...

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Veröffentlicht in:Drug and alcohol dependence 2005-09, Vol.79 (3), p.343-350
Hauptverfasser: Manrique, Héctor M., Miquel, Marta, Aragon, Carlos M.G.
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Aragon, Carlos M.G.
description The involvement of catalase in ethanol-induced locomotion has been clearly proven. However, studies addressing the role of this enzyme in the effects that ethanol exerts on memory are lacking. In the present study, the social recognition test (SRT) was used to evaluate ethanol effects on memory. In this test, the reduction in investigation time of a juvenile conspecific, when this social stimulus is presented for the second time, is considered a reliable index of memory. Exploration ratios (ER) were calculated to evaluate the recognition capacity of mice. Ethanol (0.0, 0.5, 1.0 or 1.5 g/kg, i.p.) was administered immediately after the first juvenile presentation, and 2 h later the juvenile was re-exposed to the adult. Additionally, adult mice received aminotriazole (AT) or sodium azide (two catalase inhibitors) 5 h or 30 min before juvenile presentation, respectively. Ethanol (1.0 and 1.5 g/kg) was able to reduce ER, indicating an improving effect on memory. This improvement was prevented by either AT or sodium azide pre-treatment. However, neither AT nor sodium azide attenuated the memory-enhancing capacity of NMDA or nicotine, suggesting a specific interaction between catalase inhibitors and ethanol in their effects on memory. The present results suggest that brain catalase activity could mediate the memory-enhancing capacity of ethanol and add further support to the idea that this enzyme mediates some of the psychopharmacological effects produced by ethanol.
doi_str_mv 10.1016/j.drugalcdep.2005.02.007
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However, studies addressing the role of this enzyme in the effects that ethanol exerts on memory are lacking. In the present study, the social recognition test (SRT) was used to evaluate ethanol effects on memory. In this test, the reduction in investigation time of a juvenile conspecific, when this social stimulus is presented for the second time, is considered a reliable index of memory. Exploration ratios (ER) were calculated to evaluate the recognition capacity of mice. Ethanol (0.0, 0.5, 1.0 or 1.5 g/kg, i.p.) was administered immediately after the first juvenile presentation, and 2 h later the juvenile was re-exposed to the adult. Additionally, adult mice received aminotriazole (AT) or sodium azide (two catalase inhibitors) 5 h or 30 min before juvenile presentation, respectively. Ethanol (1.0 and 1.5 g/kg) was able to reduce ER, indicating an improving effect on memory. This improvement was prevented by either AT or sodium azide pre-treatment. However, neither AT nor sodium azide attenuated the memory-enhancing capacity of NMDA or nicotine, suggesting a specific interaction between catalase inhibitors and ethanol in their effects on memory. 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subjects Acetaldehyde
Acetaldehyde - metabolism
Addictive behaviors
Adult and adolescent clinical studies
Amitrole - pharmacology
Animals
Behavior, Animal - drug effects
Behavior, Animal - physiology
Biological and medical sciences
Brain - enzymology
Brain catalase
Catalase - antagonists & inhibitors
Catalase - physiology
Dose-Response Relationship, Drug
Drug addiction
Ethanol
Ethanol - metabolism
Ethanol - pharmacology
Male
Medical sciences
Memory - drug effects
Memory - physiology
Mice
Models, Animal
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Recognition (Psychology) - drug effects
Recognition (Psychology) - physiology
Social Behavior
Social memory
Sodium Azide - pharmacology
Toxicology
title Brain catalase mediates potentiation of social recognition memory produced by ethanol in mice
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