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Tegmental pedunculopontine nucleus lesions do not block cocaine reward.

机译:盖骨足小神经节核损害不会阻碍可卡因的回报。

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Previous studies have implicated the tegmental pedunculopontine (TPP) nucleus in mediating the rewarding effects of opiates, food, and amphetamine, provided that animals are not in aversive motivational states induced by food--or drug--withdrawal. We wondered if bilateral TPP lesions could block the reinforcing effects of systemic cocaine in a place conditioning paradigm. Both lesioned and sham animals acquired cocaine place preferences. TPP-lesioned animals subsequently failed to acquire place preferences when conditioned with morphine, replicating previous data with TPP lesions. It is possible that our cocaine place conditioning protocol induced aversions during drug withdrawal, thus explaining the inability of TPP lesions to block conditioning. We looked for place aversions by conditioning animals at various times postinjection of cocaine. At no time point following drug withdrawal from cocaine were significant conditioned aversions observed. Cocaine's systemic motivational effects are mediated by asubstrate separate from the TPP substrate underlying the rewarding effects of opiates, food, and amphetamine.
机译:前提是动物没有处于因食物或药物戒断而引起的厌恶动机状态下,以前的研究已经牵涉到被盖足动物的足小核蛋白(TPP)核介导鸦片,食物和苯丙胺的奖励作用。我们想知道双边TPP病变是否可以在场所条件范式中阻断全身可卡因的增强作用。病变动物和假动物都获得了可卡因位置偏好。 TPP损伤的动物随后在使用吗啡进行调理后未能获得位置偏好,从而复制了TPP损伤的先前数据。我们的可卡因位置调节方案可能会在停药期间引起厌恶感,从而解释了TPP病变无法阻断调节作用。我们在注射可卡因后的不同时间通过调节动物来寻找地方厌恶。从可卡因撤药后的任何时间均未观察到明显的条件厌恶。可卡因的全身性激励作用是由与TPP基质分开的基质(潜在鸦片,食物和苯丙胺的奖励作用)介导的。

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