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首页> 外文期刊>Addiction biology >Oleoylethanolamide dose-dependently attenuates cocaine-induced behaviours through a PPARα receptor-independent mechanism
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Oleoylethanolamide dose-dependently attenuates cocaine-induced behaviours through a PPARα receptor-independent mechanism

机译：油酰乙醇酰胺通过PPARα受体非依赖性机制可剂量依赖性地减弱可卡因诱导的行为

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摘要

Oleoylethanolamide (OEA) is an acylethanolamide that acts as an agonist of nuclear peroxisome proliferator-activated receptor alpha (PPARα) to exert their biological functions, which include the regulation of appetite and metabolism. Increasing evidence also suggests that OEA may participate in the control of reward-related behaviours. However, direct experimental evidence for the role of the OEA-PPARα receptor interaction in drug-mediated behaviours, such as cocaine-induced behavioural phenotypes, is lacking. The present study explored the role of OEA and its receptor PPARα on the psychomotor and rewarding responsiveness to cocaine using behavioural tests indicative of core components of addiction. We found that acute administration of OEA (1, 5 or 20 mg/kg, i.p.) reduced spontaneous locomotor activity and attenuated psychomotor activation induced by cocaine (20 mg/kg) in C57Bl/6 mice. However, PPARα receptor knockout mice showed normal sensitization, although OEA was capable of reducing behavioural sensitization with fewer efficacies. Furthermore, conditioned place preference and reinstatement to cocaine were intact in these mice. Our results indicate that PPARα receptor does not play a critical, if any, role in mediating short- and long-term psychomotor and rewarding responsiveness to cocaine. However, further research is needed for the identification of the targets of OEA for its inhibitory action on cocaine-mediated responses.
机译：油酰基乙醇酰胺（OEA）是一种酰基乙醇酰胺，可作为核过氧化物酶体增殖物激活受体α（PPARα）的激动剂发挥其生物学功能，包括调节食欲和代谢。越来越多的证据还表明，OEA可能参与了与奖励相关的行为的控制。但是，缺乏直接的实验证据来证明OEA-PPARα受体相互作用在药物介导的行为（例如可卡因诱导的行为表型）中的作用。本研究使用指示成瘾的核心成分的行为测试探索了OEA及其受体PPARα在精神运动和奖励对可卡因的反应中的作用。我们发现，在C57Bl / 6小鼠中，急性给药OEA（1、5或20 mg / kg，腹膜内）降低了可卡因（20 mg / kg）诱导的自发运动活性并减弱了精神运动激活。但是，尽管OEA能够以较低的效率降低行为致敏性，但PPARα受体敲除小鼠表现出正常的致敏性。此外，在这些小鼠中完整的条件位置偏好和恢复为可卡因。我们的结果表明，PPARα受体在介导短期和长期的精神运动和奖励对可卡因的反应中不发挥关键作用（如果有的话）。但是，需要进一步的研究来鉴定OEA对可卡因介导的反应具有抑制作用的靶标。

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