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Cocaine is self-administered into the shell but not the core of the nucleus accumbens of wistar rats.

机译:可卡因是自我管理的,但不是wistar大鼠伏隔核的核心。

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The rewarding properties of cocaine have been postulated to be regulated, in part, by the mesolimbic dopamine system. However, the possibility that the rewarding properties of cocaine are mediated by direct activation of this system has yielded contradictory findings. The intracranial self-administration technique is used to identify specific brain regions involved in the initiation of response-contingent behaviors for the delivery of a reinforcer. The present study assessed whether adult Wistar rats would self-administer cocaine directly into the nucleus accumbens shell (AcbSh) and core (AcbC). For each subregion, subjects were placed in standard two-lever operant chambers and randomly assigned to one of five groups for each site that were given either artificial cerebrospinal fluid (aCSF), or 400, 800, 1200, or 1600 pmol of cocaine/100 nl to self-administer. The data indicate that rats with placements within the AcbSh readily self-administered 800 to 1600 pmol of cocaine/100 nl and responded significantly more on the active than inactive lever. These subjects also decreased responding on the active lever when aCSF was substituted for cocaine and reinstated responding on the active lever when cocaine was reintroduced. Coinfusion of the D(2)-like receptor antagonist sulpiride inhibited cocaine self-infusion in the AcbSh. In contrast to the AcbSh data, rats failed to self-administer any tested dose of cocaine into the AcbC or areas ventral to the AcbSh. These findings suggest that the AcbSh is a neuroanatomical substrate for the reinforcing effects of cocaine and that activation of D2-like receptors is involved.
机译:假定可卡因的有益特性部分受到中脑边缘多巴胺系统的调节。然而,可卡因的有益特性是由该系统的直接激活介导的,这产生了矛盾的发现。颅内自我管理技术用于识别参与响应性行为启动增强剂的特定大脑区域。本研究评估了成年Wistar大鼠是否会自行直接向可伏伏核壳(AcbSh)和核心(AcbC)内自我施用可卡因。对于每个子区域,将受试者置于标准的两杆手术室中,并随机分配给每个部位的五个组之一,分别给予人工脑脊髓液(aCSF)或400、800、1200或1600 pmol可卡因/ 100自我管理。数据表明,在AcbSh内放置的大鼠可以很容易地自我给药800至1600 pmol可卡因/ 100 nl,并且对活跃杠杆的反应明显大于非活跃杠杆。当用aCSF代替可卡因时,这些受试者的活动杠杆反应也降低,而重新引入可卡因后,这些受试者的活动杠杆反应也恢复了。 D(2)样受体拮抗剂舒必利的共注入抑制了AcbSh中的可卡因自注入。与AcbSh数据相反,大鼠未能在AcbC或AcbSh腹侧区域自行施用任何可测剂量的可卡因。这些发现表明AcbSh是可卡因增强作用的神经解剖学底物,并且涉及D2样受体的激活。

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