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Titel och upphov Predisposition to high ethanol drinking : role of ethanol reward, and relationship to central control of eating and aggressiveness in rodents
Utgivning, distribution etc.
Fysisk beskrivning
Anmärkning: Allmän
Anmärkning: Innehållsbeskrivning, sammanfattning In the present study ethanol-preferring AA and ethanol-avoiding ANA rats, and normal Swiss-Webster mice were used as models of innate and acquired predisposition to high ethanol drinking, respectively. It was hypothesized that 1) the AA rats are innately sensitive to ethanol reward, 2) mice can be rendered sensitive to ethanol reward through social deprivation, after which 3) a "rewarding" dose of ethanol might further increase aggressiveness, and 4) there could be functional differences in the central control of eating between the AA and the ANA rats. These hypotheses were tested in the following studies. A novel method was developed for automatic recording of locomotor activity of mice and rats, and of murine fighting behavior. In summary, the results support the hypothesis that the ethanol-preferring AA rats are innately sensitive to the rewarding properties of ethanol, and suggest that the AA rats differ from ANA rats in their central control of food intake. Social deprivation seems to sensitize mice to ethanol reward, presumably predisposing to high ethanol intake, but ethanol does not seem to further increase aggression in deprived mice. In general, the view that predisposition to high ethanol drinking, eating disorders, and aggression may be associated with each other at the level of sensitized brain reward mechanisms is supported.
Term
Indexterm - Okontrollerad
*000 am
*00117135
*008070120|1993|||||||||||e|m||||||||0|eng|d
*02000$z951-8913-59-3
*1001 $aPäivärinta, Petri
*24510$aPredisposition to high ethanol drinking :$brole of ethanol reward, and relationship to central control of eating and aggressiveness in rodents
*260 $aHelsinki,$c1993$y1993
*300 $a71 s :$bill.
*500 $aDiss. Helsinki : Univ.
*520 $aIn the present study ethanol-preferring AA and ethanol-avoiding ANA rats, and normal Swiss-Webster mice were used as models of innate and acquired predisposition to high ethanol drinking, respectively. It was hypothesized that 1) the AA rats are innately sensitive to ethanol reward, 2) mice can be rendered sensitive to ethanol reward through social deprivation, after which 3) a "rewarding" dose of ethanol might further increase aggressiveness, and 4) there could be functional differences in the central control of eating between the AA and the ANA rats. These hypotheses were tested in the following studies. A novel method was developed for automatic recording of locomotor activity of mice and rats, and of murine fighting behavior. In summary, the results support the hypothesis that the ethanol-preferring AA rats are innately sensitive to the rewarding properties of ethanol, and suggest that the AA rats differ from ANA rats in their central control of food intake. Social deprivation seems to sensitize mice to ethanol reward, presumably predisposing to high ethanol intake, but ethanol does not seem to further increase aggression in deprived mice. In general, the view that predisposition to high ethanol drinking, eating disorders, and aggression may be associated with each other at the level of sensitized brain reward mechanisms is supported.
*650 4$aAlcohol, ethyl
*650 4$aReinforcement (psychology)
*650 4$aReward
*650 4$aSocial isolation
*650 4$aAggression
*650 4$aEating disorders
*650 4$aAnimal
*650 4$aDopamine
*650 4$aSerotonin
*650 4$aNorepinephrine
*650 4$aRats
*650 4$aMice
*650 4$aGenetics
*653 $aAlkohol
*653 $aDjurförsök
*653 $aGenetik
*653 $aÄtstörningar
*852 $hDiss.198
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