在啮齿动物触摸屏概率奖励任务中,计算模型能区分学习率和早期生活逆境造成的奖励敏感性缺陷

IF 4 Q2 NEUROSCIENCES
Brian D. Kangas , Yuen-Siang Ang , Annabel K. Short , Tallie Z. Baram , Diego A. Pizzagalli
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引用次数: 0

摘要

背景早年遭遇逆境,包括不可预测的环境,与成年后的神经精神疾病有关。这种后遗症的一个共同因素是失乐症,即对以前具有强化作用的刺激失去反应能力。为了加快开发新的治疗策略来治疗早年逆境引起的失认症,人们开发了动物模型来捕捉早年生活压力的关键特征以及这种压力诱发的行为缺陷。为了测试这一转化平台的定量限制,我们检验了贝叶斯计算建模和概率分析的能力,它们与之前人类研究中优化的方法相同,能够精确地量化导致这些缺陷的假定机制。结果奖赏敏感性的显著缺陷(而非学习率)导致了暴露于早期生活逆境中的大鼠的厌食表型。结论目前的研究结果证实了计算建模在区分奖赏敏感性和学习率的独立特征方面的有效性,这些特征补充了概率奖赏任务的信号检测终点,从而证实并扩展了这些啮齿类动物模型的转化价值。这些指标共同作用,客观地量化了与失认症表型相关的强化学习缺陷。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Computational Modeling Differentiates Learning Rate From Reward Sensitivity Deficits Produced by Early-Life Adversity in a Rodent Touchscreen Probabilistic Reward Task

Background

Exposure to adversity, including unpredictable environments, during early life is associated with neuropsychiatric illness in adulthood. One common factor in this sequela is anhedonia, the loss of responsivity to previously reinforcing stimuli. To accelerate the development of new treatment strategies for anhedonic disorders induced by early-life adversity, animal models have been developed to capture critical features of early-life stress and the behavioral deficits that such stressors induce. We have previously shown that rats exposed to the limited bedding and nesting protocol exhibited blunted reward responsivity in the probabilistic reward task, a touchscreen-based task reverse translated from human studies.

Methods

To test the quantitative limits of this translational platform, we examined the ability of Bayesian computational modeling and probability analyses identical to those optimized in previous human studies to quantify the putative mechanisms that underlie these deficits with precision. Specifically, 2 parameters that have been shown to independently contribute to probabilistic reward task outcomes in patient populations, reward sensitivity and learning rate, were extracted, as were trial-by-trial probability analyses of choices as a function of the preceding trial.

Results

Significant deficits in reward sensitivity, but not learning rate, contributed to the anhedonic phenotypes in rats exposed to early-life adversity.

Conclusions

The current findings confirm and extend the translational value of these rodent models by verifying the effectiveness of computational modeling in distinguishing independent features of reward sensitivity and learning rate that complement the probabilistic reward task’s signal detection end points. Together, these metrics serve to objectively quantify reinforcement learning deficits associated with anhedonic phenotypes.

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来源期刊
Biological psychiatry global open science
Biological psychiatry global open science Psychiatry and Mental Health
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