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Arginine vasopressin and a vasopressin antagonist peptide: Opposite effects on extinction of active avoidance in rats
Authors:George F. Koob  Michel Le Moal  Oedile Gaffori  Maurice Manning  Wilbur H. Sawyer  Jean Rivier  Floyd E. Bloom
Affiliation:1. A.V. Davis Center for Behavioral Neurobiology, The Salk Institute, P.O. Box 85800, San Diego, CA 92138, U.S.A.;2. Laboratoire de Neurobilogie des Compartements, Université de Bordeaux II, F-33076 Bordeaux, France;3. Department of Biochemistry, Medical College of Ohio, Toledo, OH 43699, U.S.A.;4. Department of Pharmacology, College of Physicians, Columbia University, New York, NY 10032, U.S.A.;5. Peptide Biology Laboratory, The Salk Institute, P.O. Box 85800, San Diego, CA 92138, U.S.A.
Abstract:Systemic injection of arginine vasopressin (AVP) (1 μ/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)-tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5:1. At a dose of 100 μ/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction. Injections of dPTyr-(Me)AVP into the lateral ventricle were ineffective except at a dose of 10 μg/rat. These results confirm previous reports of the effect of vasopressin on delaying extinction of avoidance behavior, but suggest a site of action distant from the lateral ventricle.
Keywords:arginine vasopressin  vasopressin antagonist peptide  effects  extinction  active avoidance
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