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Suppression of drinking by naloxone in the rat: A further characterization

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Abstract

The effect of naloxone, an opiate antagonist, were examined on drinking induced by various dipsogenic stimuli. In rats deprived of water for 24 h, naloxone (0.1-10 mg/kg) produced a dose-related suppression of drinking immediately following water presentation but did not alter the latency to begin drinking. Naloxone also produced a dose-related suppression of water consumption induced by isoproterenol and angiotensin II, agents simulating conditions of extracellular dehydration. Naltrexone, a congener of naloxone, was more potent than naloxone in reducing isoproterenol-induced water intake. Schedule-induced polydipsia, which occurs in the absence of body fluid deficits, was not altered by either naloxone or naltrexone at doses attenuating drinking induced by the other methods. These data suggest that the suppressant effects of naloxone on water consumption are not a manifestation of an increased latency to drink or an impairment in the motor components of drinking activity. Futthermore, narcotic antagonists appear to attenuate regulatory, but not adjunctive drinking.

Original languageEnglish (US)
Pages (from-to)331-340
Number of pages10
JournalEuropean Journal of Pharmacology
Volume69
Issue number3
DOIs
StatePublished - Jan 29 1981

Bibliographical note

Funding Information:
* A preliminary report of this investigation was presented at the 64th annual meeting of the Federation of American Societies for Experimental Biology, and appears in Fedn. Proc. 39, 995 (1980). This investigation was supported in part by USPHS grants T01 GM00179, DA00541, and by Research Scientist Development Award K02 DA00008 to S.G.H. ** Present address: Department of Pharmacological and Physiological Sciences, University of Chicago, 947 E. 58th Street, Chicago, Illinois 60637. *** To whom correspondence should he sent.

Keywords

  • Drinking
  • Endorphins
  • Extracellular dehydration
  • Naloxone
  • Naltrexone
  • Schedule-induced polydipsia
  • Water deprivation

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