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首页> 外文期刊>Psychopharmacology >Naltrexone pretreatment decreases the reinforcing effectiveness of ethanol and saccharin but not PCP or food under concurrent progressive-ratio schedules in rhesus monkeys.
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Naltrexone pretreatment decreases the reinforcing effectiveness of ethanol and saccharin but not PCP or food under concurrent progressive-ratio schedules in rhesus monkeys.

机译:纳曲酮预处理降低了恒河猴在同时进行的进食比例时对乙醇和糖精的增强效果,但不降低PCP或食物的增强效果。

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摘要

The purpose of this experiment was to determine whether attenuation of ethanol consumption by naltrexone is the result of selective changes in the reinforcing effectiveness of drug and non-drug reinforcers. A range of naltrexone doses (0.1-1.0 mg/kg) was administered for 5 days, and the effects on the reinforcing effects of orally delivered 8% (w/v) ethanol, 0.25 mg/ml phencyclidine (PCP), 0.03% (w/v) saccharin and food were studied in eight rhesus monkeys. Food and liquids were available under independent and concurrent progressive-ratio (PR) schedules (ratio range 8-4096) during daily 3-h sessions. Ethanol-maintained responding was attenuated by 0.3 and 1.0 mg/kg doses of naltrexone, while saccharin-maintained responding was decreased at the 1.0 mg/kg dose. Furthermore, there was a significant linear trend that consumption of available ethanol and saccharin was attenuated dose-dependently by naltrexone. Following 5 days of naltrexone pretreatment, ethanol- and saccharin-maintained responding immediately returned to or exceeded baseline levels. Food- and PCP-maintained responding and intake were not significantly affected by any of the naltrexone doses examined. The decreased break point (BP) values for ethanol and saccharin suggest that their reinforcing effects are mediated through opioid reinforcement mechanisms. The lack of naltrexone attenuation of PCP- and food-maintained responding suggests that these reinforcers: 1) are not sensitive to naltrexone antagonism at the doses examined, 2) are mediated by non-opioid reinforcement mechanisms, and/or 3) have less intrinsic palatability.
机译:该实验的目的是确定纳曲酮对乙醇消耗的减少是否是药物和非药物增强剂增强效果的选择性变化的结果。给予一系列纳曲酮剂量(0.1-1.0 mg / kg),持续5天,对口服8%(w / v)乙醇,0.25 mg / ml苯环利定(PCP),0.03%( w / v)糖精和食物在八只恒河猴中进行了研究。在每天3小时的会议中,可以根据独立的并发的渐进比率(PR)计划(比率范围8-4096)获得食物和液体。乙醇维持的反应减弱为0.3和1.0 mg / kg剂量的纳曲酮,而糖精维持的响应降低为1.0 mg / kg剂量。此外,存在明显的线性趋势,纳曲酮剂量依赖性地减少了可用乙醇和糖精的消耗。纳曲酮预处理5天后,乙醇和糖精维持的反应立即恢复或超过基线水平。食物和五氯苯酚维持的反应和摄入量不受任何纳曲酮剂量的显着影响。乙醇和糖精的折断点(BP)值降低,表明它们的增强作用是通过阿片类药物的增强机制介导的。缺乏纳曲酮对PCP和食物维持反应的缓解作用表明,这些增强剂:1)在所检查的剂量下对纳曲酮拮抗作用不敏感; 2)由非阿片类药物增强机制介导,和/或3)内在作用较少适口性。

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