Involvement of opioid mu 1 receptors in morphine-induced conditioned place preference in rats
Involvement of opioid mu 1 receptors in morphine-induced conditioned place preference in rats
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DOI：
10.1016/s0091-3057(96)00567-9
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发表时间：
1997-09-01
影响因子：
3.6
通讯作者：
Ahtee, L
中科院分区：
文献类型：
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作者：
Piepponen, TP;Kivastik, T;Ahtee, L
本研究的主要目的是评价μ 1-阿片受体在吗啡奖赏中的作用。因此，我们研究了μ 1选择性拮抗剂纳洛嗪[15 mg/kg腹腔注射（IP）]拮抗吗啡[3 mg/kg皮下注射（SC）]诱导的条件性位置偏爱（CPP）的能力。此外，还研究了纳洛嗪对吗啡诱导的僵住症（15 mg/kg）、镇痛（3 mg/kg）和体温过高（3 mg/kg）的影响。为了比较，研究了非选择性阿片受体拮抗剂纳曲酮（2.5 mg/kg SC）和选择性δ阿片受体拮抗剂纳曲吲哚（2 mg/kg IF）对吗啡诱导的CPP的影响。吗啡诱导的CPP明显拮抗纳洛嗪和纳洛酮预处理（12小时和20分钟前吗啡，分别），但不纳曲吲哚（吗啡前15分钟）。纳洛嗪也拮抗吗啡诱导的僵硬和镇痛，但不吗啡诱导的体温过高。纳曲林多没有改变吗啡诱导的僵住症。这些结果表明，μ 1-阿片受体在吗啡奖励的积极作用，而吗啡诱导的体温过高似乎不介导μ 1-阿片受体。此外，δ-阿片受体似乎没有意义的吗啡诱导的奖励。(C)1997年爱思唯尔科学公司
The main purpose of this study was to evaluate the role of mu 1-opioid receptors in morphine reward. Therefore, we studied the ability of a mu 1-selective antagonist, naloxonazine [15 mg/kg intraperitoneally (IP)], to antagonize the conditioned place preference (CPP) induced by morphine [3 mg/kg subcutaneously (SC)]. In addition, effects of naloxonazine on morphine-induced catalepsy (15 mg/kg), analgesia (3 mg/kg), and hyperthermia (3 mg/kg) were studied. For comparison, the effects of a nonselective opioid receptor antagonist, naltrexone (2.5 mg/kg SC), and a selective delta-opioid receptor antagonist, naltrindole (2 mg/kg IF), on CPP induced by morphine were investigated. Morphine-induced CPP was clearly antagonized by pretreatment with naloxonazine and naltrexone (12 h and 20 min prior to morphine, respectively) but not by naltrindole (15 min before morphine). Naloxonazine also antagonized morphine-induced catalepsy and analgesia but not morphine-induced hyperthermia. Naltrindore did not modify morphine-induced catalepsy. These results suggest an active role for mu 1-opioid receptors in morphine reward, whereas morphine-induced hyperthermia does not appear to be mediated by mu 1-opioid receptors. Furthermore, delta-opioid receptors seem to be without significance in morphine-induced reward. (C) 1997 Elsevier Science Inc.