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首页> 外文期刊>The European Journal of Neuroscience >Abnormal associative encoding in orbitofrontal neurons in cocaine-experienced rats during decision-making.
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Abnormal associative encoding in orbitofrontal neurons in cocaine-experienced rats during decision-making.

机译：可卡因经验丰富的大鼠在决策过程中眶额神经元的异常关联编码。

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Recent evidence has linked exposure to addictive drugs to an inability to employ information about adverse consequences, or outcomes, to control behavior. For instance, addicts and drug-experienced animals fail to adapt their behavior to avoid adverse outcomes in gambling and reversal tasks or after changes in the value of expected rewards. These deficits are similar to those caused by damage to the orbitofrontal cortex, suggesting that addictive drugs may cause long-lasting changes in the representation of outcome associations in a circuit that includes the orbitofrontal cortex. Here we test this hypothesis by recording from orbitofrontal neurons in a discrimination task in rats previously exposed to cocaine (30 mg/kg i.p. for 14 days). We found that orbitofrontal neurons recorded in cocaine-experienced rats failed to signal the adverse outcome at the time a decision was made in the task. The loss of this signal was associated with abnormal changes in response latencies on aversive trials. Furthermore, upon reversal of the cue-outcome associations, orbitofrontal neurons in cocaine-treated rats with enduring reversal impairments failed to reverse their cue-selectivity, while orbitofrontal neurons in cocaine-treated rats with normal performance showed an increase in the plasticity of cue-selective firing after reversal. These results provide direct neurophysiological evidence that exposure to cocaine can cause behaviorally relevant changes in the processing of associative information in a circuit that includes the orbitofrontal cortex.
机译：最近的证据表明，接触成瘾性药物与无法利用有关不良后果或后果的信息来控制行为有关。例如，成瘾者和有吸毒经验的动物无法适应其行为，从而避免在赌博和逆转任务中或预期奖励价值发生变化后产生不利后果。这些缺陷类似于由眶额皮质损害引起的缺陷，表明成瘾药物可能导致包括眶额皮质在内的回路中结局关联的代表出现长期变化。在这里，我们通过在先前暴露于可卡因（30 mg / kg i.p.，持续14天）的大鼠的辨别任务中记录眶额神经元来检验该假设。我们发现在可卡因有经验的大鼠中记录的眶额神经元未能在任务中做出决定时预示不良结果。该信号的丧失与厌恶试验中反应潜伏期的异常变化有关。此外，在提示-结果关联发生逆转时，可卡因治疗的持久逆转损伤大鼠的眶额神经元不能逆转其提示选择性，而可卡因治疗的具有正常表现的大鼠的眶额神经元显示出提示-可塑性的增加反转后的选择性射击。这些结果提供了直接的神经生理学证据，表明可卡因的暴露会在包括眶额皮质的回路中引起相关信息处理过程中的行为相关变化。

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