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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Continuous intracerebroventricular infusion of the competitive NMDA receptor antagonist, LY235959, facilitates escalation of cocaine self-administration and increases break point for cocaine in Sprague-Dawley rats.
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Continuous intracerebroventricular infusion of the competitive NMDA receptor antagonist, LY235959, facilitates escalation of cocaine self-administration and increases break point for cocaine in Sprague-Dawley rats.

机译：竞争性NMDA受体拮抗剂LY235959的连续脑室内注入可卡因可自行给药，并增加了Sprague-Dawley大鼠的可卡因断裂点。

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摘要

Although escalation of consumption is an important characteristic of cocaine dependence, the neurobiological mechanisms that mediate this phenomenon have not been fully described. In this study, we used male, Sprague-Dawley rats to measure the effects of acute and continuous intracerebroventricular (ICV) administration of the competitive NMDA receptor antagonist, LY235959, on cocaine self-administration behavior under various schedules of reinforcement and access conditions. Single ICV infusions of LY235959 (0.03-0.3 microg/5 microl) produced dose-dependent and statistically significant decreases in the number of cocaine infusions earned under a progressive ratio schedule of reinforcement. In a second experiment, vehicle or LY235959 (0.2-0.3 microg/day) was continuously administered ICV to rats via surgically-implanted subcutaneous osmotic minipump/intracranial cannula assemblies. Both vehicle- and LY235959-treated rats significantly escalated cocaine self-administration over the 10 long access sessions; however, rats treated with LY235959 escalated cocaine self-administration faster and to a greater degree than vehicle-treated rats. There was a statistically significant increase in cocaine infusions earned under the PR schedule in LY235959-treated rats, but not vehicle-treated rats, after 10 long access cocaine self-administration sessions. These data support the hypothesis that escalation of cocaine consumption is mediated by hypo-glutamatergic tone in the central nervous system and this facilitation of escalation is associated with an increase in motivation to respond for cocaine.
机译：尽管消耗量的增加是可卡因依赖性的重要特征，但尚未充分描述介导此现象的神经生物学机制。在这项研究中，我们使用雄性Sprague-Dawley大鼠测量了在不同强化和进入条件下，急性和连续性脑室内（ICV）施用竞争性NMDA受体拮抗剂LY235959对可卡因自我施用行为的影响。 LY235959（0.03-0.3 microg / 5 microl）的单次ICV输注产生剂量依赖性，并在逐步加强配比方案下获得可卡因输注次数的统计显着减少。在第二个实验中，通过手术植入的皮下渗透性微型泵/颅内插管组件向大鼠连续施用媒介物或LY235959（0.2-0.3微克/天）ICV。用媒介物和LY235959治疗的大鼠在10次长距离接触中可卡因的自我给药均显着升高。然而，与媒介物治疗的大鼠相比，用LY235959治疗的大鼠可卡因自我管理的给药速度更快，而且程度更高。经过10次长期可卡因自我管理后，在PR时间表下，接受LY235959治疗的大鼠，但未接受赋形剂治疗的大鼠，可卡因的输注有统计上的显着增加。这些数据支持以下假设：可卡因消费量的增加是由中枢神经系统中的低谷氨酸能介导的，这种促进作用与对可卡因作出反应的动机增加有关。

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