Department of Psychology, University of Maryland, College Park, Maryland 20742
Program in Neuroscience and Cognitive Science, University of Maryland, College Park, Maryland 20742.
J Neurosci. 2021 May 26;41(21):4667-4677. doi: 10.1523/JNEUROSCI.3025-20.2021. Epub 2021 Apr 13.
The insula contributes to behavioral control and is disrupted by substance abuse, yet we know little about the neural signals underlying these functions or how they are disrupted after chronic drug self-administration. Here, male and female rats self-administered either cocaine (experimental group) or sucrose (control) for 12 consecutive days. After a 1 month withdrawal period, we recorded from insula while rats performed a previously learned reward-guided decision-making task. Cocaine-exposed rats were more sensitive to value manipulations and were faster to respond. These behavioral changes were accompanied by elevated counts of neurons in the insula that increased firing to reward. These neurons also fired more strongly at the start of long-delay trials, when a more immediate reward would be expected, and fired less strongly in anticipation of the actual delivery of delayed rewards. Although reward-related firing to immediate reward was enhanced after cocaine self-administration, reward-predicting cue and context signals were attenuated. In addition to revealing novel firing patterns unique to insula, our data suggest changes in such neural activity likely contribute to impaired decision making observed after drug use. The insula plays a clear role in drug addiction and drug-induced impairments of decision making, yet there is little understanding of its underlying neural signals. We found that chronic cocaine self-administration reduces cue and context encoding in insula while enhancing signals related to immediate reward. These changes in neural activity likely contribute to impaired decision making and impulsivity observed after drug use.
脑岛参与行为控制，并且会受到物质滥用的干扰，但我们对于这些功能的神经信号知之甚少，也不知道它们在慢性药物自我给药后是如何被破坏的。在这里，雄性和雌性大鼠连续 12 天自行给予可卡因（实验组）或蔗糖（对照组）。在 1 个月的戒断期后，我们在大鼠进行先前学习的奖励导向决策任务时记录脑岛的神经活动。暴露于可卡因的大鼠对价值操纵更为敏感，反应速度也更快。这些行为变化伴随着脑岛中神经元数量的增加，这些神经元对奖励的反应更为活跃。这些神经元在长时延迟试验开始时也会更强烈地发射，此时预计会有更直接的奖励，而在期待延迟奖励的实际发放时则发射得较弱。尽管可卡因自我给药后，与即时奖励相关的神经活动增强，但与奖励预测相关的线索和背景信号减弱。除了揭示脑岛特有的新的发射模式外，我们的数据还表明，这种神经活动的变化可能导致药物使用后观察到的决策能力受损。脑岛在药物成瘾和药物引起的决策障碍中起着明显的作用，但对其潜在的神经信号知之甚少。我们发现，慢性可卡因自我给药会减少脑岛中的线索和背景编码，同时增强与即时奖励相关的信号。这些神经活动的变化可能导致药物使用后观察到的决策能力受损和冲动。
