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不同的中枢阿片受体亚型拮抗剂可改变假饲和假饮大鼠中麦芽糖糊精和剥夺诱导的水摄入量。

Different central opioid receptor subtype antagonists modify maltose dextrin and deprivation-induced water intake in sham feeding and sham drinking rats.

作者信息

Leventhal L, Bodnar R J

机构信息

Department of Psychology, Queens College, City University of New York, Flushing 11367, USA.

出版信息

Brain Res. 1996 Nov 25;741(1-2):300-8. doi: 10.1016/s0006-8993(96)00951-1.

Abstract

Different central opioid receptor subtypes participate in the mediation of intakes of simple (sucrose: mu, kappa 1) and complex (maltose dextrin: mu) carbohydrates as well as deprivation-induced water intake (mu) under real-feeding and real-drinking conditions. An identical pattern of mu and kappa 1 mediation of sucrose intake was observed in sham-feeding rats as well, suggesting their actions on orosensory mechanisms supporting sucose intake. The present study examined whether centrally administered general (naltrexone: 1-50 micrograms), mu (beta-funaltrexamine: 1-20 micrograms), mu 1 (naloxonazine: 50 micrograms), kappa 1 (nor-binaltorphamine: 1-20 micrograms), delta 1 ([D-Ala2, Leu5, Cys6]-enkephalin: 10-40 micrograms) or delta 2 (naltrindole isothiocyanate: 20 micrograms) opioid subtype antagonists altered either maltose dextrin (10%) intake during sham feeding or deprivation (24 h)-induced water intake during sham drinking in rats with gastric fistulas. Sham feeding significantly increased maltose dextrin intake (180%) and sham drinking significantly increased deprivation-induced water intake (256%) over a 60 min time course. Naltrexone significantly and dose-dependently reduced maltose dextrin intake (78%) in sham feeding rats, and deprivation-induced water intake (51%) in sham drinking rats. Maltose dextrin intake in sham feeding rats was significantly reduced by either kappa 1 (69%) or delta 1 (59%) opioid antagonism, was significantly increased by mu 1 antagonism (43%), and was not significantly affected by either mu or delta 2 opioid antagonism. Deprivation-induced water intake in sham drinking rats was significantly reduced by either mu (41%), mu 1 (28%), delta 1 (48%) or delta 2 (28%) opioid antagonism, but was not significantly affected by kappa 1 opioid antagonism. The difference in opioid receptor subtype mediation of maltose dextrin intake in real feeding and sham feeding conditions suggest that kappa 1 and delta 1 receptors are involved in the orosensory mechanisms supporting maltose dextrin intake, while mu receptors are involved in the ingestive and post-ingestive mechanisms supporting maltose dextrin intake. The different patterns of opioid involvement in sucrose and maltose dextrin intake in sham feeding and real feeding conditions provide further support for the hypothesis that at least two different carbohydrate taste systems exist. The difference in opioid receptor subtype mediation of deprivation-induced water intake in real drinking and sham drinking conditions may reflect the removal in the sham drinking condition of a mu-mediated prerestorative satiety mechanism, and the unmasking of other opioid-mediated signalling mechanisms.

摘要

在实际进食和饮水条件下,不同的中枢阿片受体亚型参与介导简单碳水化合物(蔗糖:μ、κ1)和复合碳水化合物(麦芽糖糊精:μ)的摄入以及剥夺诱导的水摄入(μ)。在假饲大鼠中也观察到了蔗糖摄入的μ和κ1介导的相同模式,表明它们对支持蔗糖摄入的口感觉机制有作用。本研究考察了中枢给予一般的(纳曲酮:1 - 50微克)、μ(β-氟纳曲明:1 - 20微克)、μ1(纳洛嗪:50微克)、κ1(去甲双氢吗啡酮:1 - 20微克)、δ1([D - Ala2,Leu5,Cys6] - 脑啡肽:10 - 40微克)或δ2(异硫氰酸纳曲吲哚:20微克)阿片受体亚型拮抗剂是否会改变胃瘘大鼠假饲期间麦芽糖糊精(10%)的摄入量或假饮期间剥夺(24小时)诱导的水摄入量。在60分钟的时间过程中,假饲显著增加了麦芽糖糊精的摄入量(180%),假饮显著增加了剥夺诱导的水摄入量(256%)。纳曲酮显著且剂量依赖性地降低了假饲大鼠中麦芽糖糊精的摄入量(78%)以及假饮大鼠中剥夺诱导的水摄入量(51%)。κ1(69%)或δ1(59%)阿片受体拮抗作用显著降低了假饲大鼠中麦芽糖糊精的摄入量,μ1拮抗作用使其显著增加(43%),而μ或δ2阿片受体拮抗作用对其无显著影响。μ(41%)、μ1(28%)、δ1(48%)或δ2(28%)阿片受体拮抗作用显著降低了假饮大鼠中剥夺诱导的水摄入量,但κ1阿片受体拮抗作用对其无显著影响。实际进食和假饲条件下麦芽糖糊精摄入的阿片受体亚型介导的差异表明,κ1和δ1受体参与支持麦芽糖糊精摄入的口感觉机制,而μ受体参与支持麦芽糖糊精摄入的摄取和摄取后机制。假饲和实际进食条件下阿片类物质参与蔗糖和麦芽糖糊精摄入的不同模式为至少存在两种不同的碳水化合物味觉系统这一假说提供了进一步支持。实际饮水和假饮条件下剥夺诱导的水摄入的阿片受体亚型介导的差异可能反映了在假饮条件下μ介导的恢复前饱腹感机制的消除以及其他阿片介导的信号机制的暴露。

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