{"title":"Palatability-induced drinking after administration of morphine, naltrexone and diazepam in the non-deprived rat.","authors":"S J Cooper","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Rats consumed excessive quantities of a highly palatable 0.005M sodium saccharin solution in the absence of depletion of body fluid compartments. The taste strongly promoted drinking, and the consequent fluid consumption proved to be very sensitive to opiate receptor blockade. Naltrexone, at a dose as small as 0.03 mg/kg, significantly attenuated consumption of the saccharin solution in the first hour of access. The naltrexone treatment did not affect latency to drink, and its suppressant effect was transient, indicating that it did not induce either immediate or lasting avoidance of the saccharin solution. The naltrexone-induced suppression was also not due to elicited stress or anxiety, since concurrent administration of diazepam did not reverse the naltrexone effect. Morphine (0.3-3.0 mg/kg) failed to enhance saccharin solution intake over a 6 hr test period. Morphine (10 mg/kg) produced immobility and an extended suppression of drinking, which was followed by a secondary hyperdipsic response.</p>","PeriodicalId":22076,"journal":{"name":"Substance and alcohol actions/misuse","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Substance and alcohol actions/misuse","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Rats consumed excessive quantities of a highly palatable 0.005M sodium saccharin solution in the absence of depletion of body fluid compartments. The taste strongly promoted drinking, and the consequent fluid consumption proved to be very sensitive to opiate receptor blockade. Naltrexone, at a dose as small as 0.03 mg/kg, significantly attenuated consumption of the saccharin solution in the first hour of access. The naltrexone treatment did not affect latency to drink, and its suppressant effect was transient, indicating that it did not induce either immediate or lasting avoidance of the saccharin solution. The naltrexone-induced suppression was also not due to elicited stress or anxiety, since concurrent administration of diazepam did not reverse the naltrexone effect. Morphine (0.3-3.0 mg/kg) failed to enhance saccharin solution intake over a 6 hr test period. Morphine (10 mg/kg) produced immobility and an extended suppression of drinking, which was followed by a secondary hyperdipsic response.