Department of Psychiatry, University of Maryland School of Medicine, MD Psychiatric Research Center, P.O. Box 21247, Baltimore, MD 21228, USA.
Neuropsychology. 2011 Jan;25(1):86-97. doi: 10.1037/a0020882.
Patients with schizophrenia (SZ) show reinforcement learning impairments related to both the gradual/procedural acquisition of reward contingencies, and the ability to use trial-to-trial feedback to make rapid behavioral adjustments.
We used neurocomputational modeling to develop plausible mechanistic hypotheses explaining reinforcement learning impairments in individuals with SZ. We tested the model with a novel Go/NoGo learning task in which subjects had to learn to respond or withhold responses when presented with different stimuli associated with different probabilities of gains or losses in points. We analyzed data from 34 patients and 23 matched controls, characterizing positive- and negative-feedback-driven learning in both a training phase and a test phase.
Consistent with simulations from a computational model of aberrant dopamine input to the basal ganglia patients, patients with SZ showed an overall increased rate of responding in the training phase, together with reduced response-time acceleration to frequently rewarded stimuli across training blocks, and a reduced relative preference for frequently rewarded training stimuli in the test phase. Patients did not differ from controls on measures of procedural negative-feedback-driven learning, although patients with SZ exhibited deficits in trial-to-trial adjustments to negative feedback, with these measures correlating with negative symptom severity.
These findings support the hypothesis that patients with SZ have a deficit in procedural "Go" learning, linked to abnormalities in DA transmission at D1-type receptors, despite a "Go bias" (increased response rate), potentially related to excessive tonic dopamine. Deficits in trial-to-trial reinforcement learning were limited to a subset of patients with SZ with severe negative symptoms, putatively stemming from prefrontal cortical dysfunction.
精神分裂症（SZ）患者表现出与逐渐/程序性获得奖励关联，以及使用试次间反馈快速调整行为的能力相关的强化学习损伤。
我们使用神经计算建模来制定合理的机制假设，以解释 SZ 个体的强化学习损伤。我们使用一种新的 Go/NoGo 学习任务来测试该模型，在此任务中，受试者必须学会在呈现不同的刺激时做出反应或不反应，这些刺激与不同的点数增益或损失的概率相关。我们分析了来自 34 名患者和 23 名匹配对照者的数据，在训练阶段和测试阶段都对正反馈和负反馈驱动的学习进行了特征描述。
与基底神经节中异常多巴胺输入的计算模型的模拟结果一致，SZ 患者在训练阶段的总体反应率增加，同时在训练块中对经常奖励的刺激的反应时间加速减少，以及在测试阶段对经常奖励的训练刺激的相对偏好减少。患者在程序负反馈驱动的学习测量上与对照者没有差异，尽管 SZ 患者在对负反馈的试次间调整上存在缺陷，这些测量与阴性症状严重程度相关。
这些发现支持了这样的假设，即 SZ 患者在程序性“Go”学习中存在缺陷，这与 D1 型受体的多巴胺传递异常有关，尽管存在“Go 偏向”（反应率增加），可能与过度的紧张性多巴胺有关。试次间强化学习缺陷仅限于具有严重阴性症状的 SZ 患者的一部分，可能源于前额叶皮层功能障碍。
