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首页> 外文期刊>Addiction biology >Effects of repeated yohimbine administration on reinstatement of palatable food seeking: involvement of dopamine D-1-like receptors and food-associated cues
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Effects of repeated yohimbine administration on reinstatement of palatable food seeking: involvement of dopamine D-1-like receptors and food-associated cues

机译：反复服用育亨宾对恢复可口食物的影响：多巴胺D-1样受体的参与和与食物相关的提示

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Acute exposure to the pharmacological stressor yohimbine induces relapse to both food and drug seeking in a rat model. However, no systematic studies on the effects of chronic stress on relapse have been conducted. Because chronic stress causes changes in dopamine D-1-like receptor-mediated transmission in prefrontal cortex (a relapse node), we tested the hypothesis that chronic exposure to stress increases vulnerability to relapse via dopamine-mediated mechanisms. Additionally, to determine the role of food-conditioned cues in reinstatement of food seeking, we made discrete food-paired cues either available (CS Present) or not available (CS Absent) during extinction and reinstatement testing. Rats responded for palatable food reinforcers in daily 3-hour sessions, and the behavior was extinguished. To model chronic stress, rats were injected daily with yohimbine (0.0, 2.5, or 5.0mg/kg; i.p.) during the first 7days of extinction. Injections were combined with SCH-23390 (0.0, 5.0, or 10.0 mu g/kg; i.p.), a D-1-like receptor antagonist. Rats were then tested for reinstatement of food seeking triggered by acute yohimbine (0.0, 1.0, or 2.0mg/kg; i.p.) and pellet priming. Rats treated previously with chronic yohimbine displayed increased responding following acute yohimbine priming relative to non-chronically stressed rats, but in the CS Absent condition only. Conversely, the lower dose of chronic yohimbine caused an increase in pellet-primed reinstatement, but this effect was more pronounced in the CS Present condition. Importantly, SCH-23390 combined with repeated yohimbine injections attenuated these effects. Thus, chronic stress may increase vulnerability to relapse under specific circumstances via a dopamine D-1-like receptor-mediated mechanism.
机译：在大鼠应激模型中，急性暴露于药理应激源育亨宾可导致食物和药物寻觅复发。但是，尚未对慢性应激对复发的影响进行系统的研究。由于慢性应激会导致前额叶皮层（复发节点）中多巴胺D-1样受体介导的传递发生变化，因此我们检验了长期暴露于压力下会增加通过多巴胺介导的机制对复发的脆弱性的假设。此外，为了确定食物条件提示在恢复寻找食物中的作用，我们在消灭和恢复测试过程中使离散的食物配对提示可用（不存在CS）或不存在（不存在CS）。在每天的3小时内，大鼠对可口的食物增强剂做出了反应，并且这种行为被扑灭了。为了模拟慢性应激，在灭绝的前7天每天向大鼠注射育亨宾（0.0、2.5或5.0mg / kg;腹腔注射）。将注射液与D-1样受体拮抗剂SCH-23390（0.0、5.0或10.0μg / kg;腹腔注射）合并使用。然后测试大鼠恢复由急性育亨宾（0.0、1.0或2.0mg / kg;腹腔注射）和颗粒引发引发的食物寻找。相对于非慢性应激大鼠，先前用慢性育亨宾治疗的大鼠在急性育亨宾启动后表现出增强的反应，但仅在CS缺失的情况下。相反，较低剂量的慢性育亨宾引起了颗粒引发的恢复的增加，但是这种作用在CS现况下更为明显。重要的是，SCH-23390与反复的育亨宾注射剂相结合可减弱这些作用。因此，慢性应激可能通过多巴胺D-1样受体介导的机制增加在特定情况下复发的脆弱性。

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