TY - JOUR
T1 - Vasopressin and ethanol preference. II. Altered preference in two strains of diabetes insipidus rats and nephrogenic diabetes insipidus mice
AU - Crabbe, John C.
AU - Rigter, Henk
N1 - Funding Information:
Part of the data were reported at the International Symposium on the Brattleboro Rat, Hanover, New Hampshire, 5-7 September 1981. The authors thank Yvonne Mous and Helen Hall for secretarial assistance, Chris Dortmans, Huub Rijk, Emmett R. Young, Brenda R. Tam and Ann Kosobud for help with the experiments, and an anonymous reviewer for helpful critical comments. These experiments were supported in part by Grant AA05828 from the NIAAA to JCC.
PY - 1985
Y1 - 1985
N2 - In the first paper of this series, the influence of a single gene (di) for vasopressin deticiency on ethanol intake in rats was demonstrated. We studied preference for concentrations of ethanol between 2.2 and 10 percent versus tap water in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Treatment with vasopressin or related peptides restored ethanol drinking to normal but also corrected water balance [13]. In the experiments reported here, Roman High Avoidance (RHA) rats of three genotypes (+/+, di/+, and di/di) were also tested for ethanol intake and preference with similar but not identical results. Thus, the effects of the di gene are independent of the genetic background on which it is placed to at least some extent. Chlorothiazide, a drug unrelated to vasopressin, also normalized ethanol drinking and corrected water balance in di/di rats. In nephrogenic diabetes insipidus mice, there was a strong negative correlation between severity of polydipsia and preference for ethanol. Thus, no paradigm tested was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.
AB - In the first paper of this series, the influence of a single gene (di) for vasopressin deticiency on ethanol intake in rats was demonstrated. We studied preference for concentrations of ethanol between 2.2 and 10 percent versus tap water in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Treatment with vasopressin or related peptides restored ethanol drinking to normal but also corrected water balance [13]. In the experiments reported here, Roman High Avoidance (RHA) rats of three genotypes (+/+, di/+, and di/di) were also tested for ethanol intake and preference with similar but not identical results. Thus, the effects of the di gene are independent of the genetic background on which it is placed to at least some extent. Chlorothiazide, a drug unrelated to vasopressin, also normalized ethanol drinking and corrected water balance in di/di rats. In nephrogenic diabetes insipidus mice, there was a strong negative correlation between severity of polydipsia and preference for ethanol. Thus, no paradigm tested was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.
KW - Chlorothiazide
KW - Des-9-Glycinamide-[Arginine] vasopressin
KW - Diabetes insipidus
KW - Diurnal rhythm
KW - Ethanol preference drinking
KW - Nephrogenic diabetes insipidus
KW - Os mice
KW - Pharmacogenetics
KW - Vasopressin
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U2 - 10.1016/0196-9781(85)90171-8
DO - 10.1016/0196-9781(85)90171-8
M3 - Article
C2 - 4070023
AN - SCOPUS:0022353515
SN - 0196-9781
VL - 6
SP - 677
EP - 683
JO - Peptides
JF - Peptides
IS - 4
ER -