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首页> 外文期刊>Addiction biology >Cocaine conditioned place preference: unexpected suppression of preference due to testing combined with strong conditioning
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Cocaine conditioned place preference: unexpected suppression of preference due to testing combined with strong conditioning

机译：可卡因有条件的地方优先考虑：由于测试结合强大的调理而意外抑制偏好

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Abstract Conditioned place preference (CPP) is widely used for evaluating the rewarding effects of drugs. Like other memories, CPP is proposed to undergo reconsolidation during which it is unstable and sensitive to pharmacological inhibition. Previous studies have shown that cocaine CPP can be apparently erased by extracellular signal‐regulated kinase (ERK) pathway inhibition during cocaine reconditioning (re‐exposure to the drug‐paired environment in the presence of the drug). Here, we show that blockade of D1 receptors during reconditioning prevented ERK activation and induced a loss of CPP. However, we also unexpectedly observed a CPP disappearance in mice that underwent testing and reconditioning with cocaine alone, specifically in strong conditioning conditions. The loss was due to the intermediate test. CPP was not recovered with reconditioning or priming in the short term, but it spontaneously reappeared after a month. When we challenged the D1 antagonist‐mediated erasure, we observed that both a high dose of cocaine and a first CPP test were required for this effect. Our results also suggest a balance between D1‐dependent ERK pathway activation and an A2a‐dependent mechanism in D2 striatal neurons in controlling CPP expression. Our data reveal that, paradoxically, a simple CPP test can induce a complete (but transient) loss of place preference following strong but not weak cocaine conditioning. This study emphasizes the complex nature of CPP memory and the importance of multiple parameters that must be taken into consideration when investigating reconsolidation.
机译：摘要条件的地方偏好（CPP）广泛用于评估药物的奖励效果。与其他记忆一样，CPP被建议经过重新染色，在此期间它对药理抑制不稳定并且敏感。以前的研究表明，可卡因Cocaine CPP可以通过细胞外信号调节的激酶（ERK）途径抑制在可卡因再修复期间（在药物存在下重新接触药物配对环境）。在这里，我们表明在修复期间阻止D1受体阻止了ERK激活并引起了CPP的丧失。然而，我们也意外地观察到在单独使用可卡因进行测试和修复的小鼠中的CPP消失，特别是在强大的调理条件下。损失是由于中间试验。在短期内，CPP未被重新处理或启动恢复，但它在一个月后自发地重新出现。当我们挑战D1拮抗剂介导的擦除时，我们观察到这两种可卡因和第一个CPP测试都是这样的效果。我们的结果还表明D1依赖性ERK途径激活与D2纹纹神经元中的A2A依赖机制之间的平衡在控制CPP表达中。我们的数据揭示了，矛盾的是，简单的CPP测试可以在强大但不弱的可卡因调理后诱导完整（但瞬态）丧失的地方偏好。本研究强调了CPP存储器的复杂性，以及在调查重新掩体时必须考虑的多个参数的重要性。

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