Frank Michael J, O'Reilly Randall C
Department of Psychology and Program in NeuroscienceUniversity of Arizona, Tucson, AZ 85721, USA.
Behav Neurosci. 2006 Jun;120(3):497-517. doi: 10.1037/0735-7044.120.3.497.
The authors test a neurocomputational model of dopamine function in cognition by administering to healthy participants low doses of D2 agents cabergoline and haloperidol. The model suggests that DA dynamically modulates the balance of Go and No-Go basal ganglia pathways during cognitive learning and performance. Cabergoline impaired, while haloperidol enhanced, Go learning from positive reinforcement, consistent with presynaptic drug effects. Cabergoline also caused an overall bias toward Go responding, consistent with postsynaptic action. These same effects extended to working memory and attentional domains, supporting the idea that the basal ganglia/dopamine system modulates the updating of prefrontal representations. Drug effects interacted with baseline working memory span in all tasks. Taken together, the results support a unified account of the role of dopamine in modulating cognitive processes that depend on the basal ganglia.
作者通过给健康参与者服用低剂量的D2药物卡麦角林和氟哌啶醇，测试了一种用于认知的多巴胺功能神经计算模型。该模型表明，多巴胺在认知学习和表现过程中动态调节“去”和“不去”基底神经节通路的平衡。卡麦角林损害了从正强化中进行“去”学习的能力，而氟哌啶醇则增强了这种能力，这与突触前药物效应一致。卡麦角林还导致了对“去”反应的总体偏向，这与突触后作用一致。这些相同的效应扩展到工作记忆和注意力领域，支持了基底神经节/多巴胺系统调节前额叶表征更新的观点。在所有任务中，药物效应都与基线工作记忆广度相互作用。综合来看，这些结果支持了对多巴胺在调节依赖于基底神经节的认知过程中作用的统一解释。
