Department of Clinical Psychology, Leiden University, the Netherlands; Leiden Institute for Brain and Cognition (LIBC), Leiden, the Netherlands.
Centre for Human Brain Health, School of Psychology, University of Birmingham, Birmingham, UK; Institute for Mental Health, School of Psychology, University of Birmingham, Birmingham, UK; Centre for Developmental Science, School of Psychology, University of Birmingham, UK.
Neuroimage. 2023 Apr 15;270:119983. doi: 10.1016/j.neuroimage.2023.119983. Epub 2023 Feb 26.
Humans learn through reinforcement, particularly when outcomes are unexpected. Recent research suggests similar mechanisms drive how we learn to benefit other people, that is, how we learn to be prosocial. Yet the neurochemical mechanisms underlying such prosocial computations remain poorly understood. Here, we investigated whether pharmacological manipulation of oxytocin and dopamine influence the neurocomputational mechanisms underlying self-benefitting and prosocial reinforcement learning. Using a double-blind placebo-controlled cross-over design, we administered intranasal oxytocin (24 IU), dopamine precursor l-DOPA (100 mg + 25 mg carbidopa), or placebo over three sessions. Participants performed a probabilistic reinforcement learning task with potential rewards for themselves, another participant, or no one, during functional magnetic resonance imaging. Computational models of reinforcement learning were used to calculate prediction errors (PEs) and learning rates. Participants behavior was best explained by a model with different learning rates for each recipient, but these were unaffected by either drug. On the neural level, however, both drugs blunted PE signaling in the ventral striatum and led to negative signaling of PEs in the anterior mid-cingulate cortex, dorsolateral prefrontal cortex, inferior parietal gyrus, and precentral gyrus, compared to placebo, and regardless of recipient. Oxytocin (versus placebo) administration was additionally associated with opposing tracking of self-benefitting versus prosocial PEs in dorsal anterior cingulate cortex, insula and superior temporal gyrus. These findings suggest that both l-DOPA and oxytocin induce a context-independent shift from positive towards negative tracking of PEs during learning. Moreover, oxytocin may have opposing effects on PE signaling when learning to benefit oneself versus another.
人类通过强化学习，尤其是当结果出乎意料时。最近的研究表明，类似的机制驱动着我们如何学会为他人谋利，也就是说，我们如何学会成为亲社会的。然而，驱动这种亲社会计算的神经化学机制仍知之甚少。在这里，我们研究了神经递质催产素和多巴胺的药理学干预是否会影响自我获益和亲社会强化学习的神经计算机制。我们采用双盲安慰剂对照交叉设计，在三个疗程中分别给予鼻内催产素（24IU）、多巴胺前体 l-多巴（100mg+25mg 卡比多巴）或安慰剂。参与者在功能磁共振成像期间进行了一个潜在的自我奖励、另一个参与者奖励或无人奖励的概率强化学习任务。使用强化学习的计算模型来计算预测误差（PE）和学习率。参与者的行为最好由一个为每个接受者设置不同学习率的模型来解释，但这两种药物都没有影响。然而，在神经水平上，两种药物都使腹侧纹状体中的 PE 信号减弱，并导致前扣带皮质、背外侧前额叶皮质、下顶叶和中央前回中的 PE 信号呈负性，与安慰剂相比，无论接受者如何。与安慰剂相比，催产素（而非安慰剂）给药还与背侧前扣带皮质、岛叶和颞上回中自我获益与亲社会 PE 的相反跟踪相关。这些发现表明，l-多巴和催产素都在学习过程中导致 PE 的跟踪从积极向消极转变，这种转变不依赖于背景。此外，当学习使自己受益与使他人受益时，催产素可能对 PE 信号产生相反的影响。
