Correction: Genetic inhibition of neurotransmission reveals role of glutamatergic input to dopamine neurons in high-effort behavior.
Correction: Genetic inhibition of neurotransmission reveals role of glutamatergic input to dopamine neurons in high-effort behavior.
复制标题
纠正：神经传递的基因抑制揭示了谷氨酸能输入多巴胺神经元在高努力行为中的作用。
DOI：
10.1038/mp.2018.3
复制
发表时间：
2018
影响因子：
11
通讯作者：
Lu,W
中科院分区：
文献类型：
--
作者：
Hutchison,MA;Gu,X;Adrover,MF;Lee,MR;Hnasko,TS;Alvarez,VA;Lu,W
中脑多巴胺神经元对许多行为和认知功能至关重要。多巴胺能传入作为主要的兴奋性输入，对多巴胺神经元的活动和可塑性的控制起着重要作用。然而，多巴胺能输入作为一个整体对多巴胺神经元的作用仍然不清楚。在这里，我们开发了一种小鼠品系，其中多巴胺神经元的多巴胺能输入被特异性地损害，并利用这种遗传模型来直接测试多巴胺能输入在多巴胺相关功能中的作用。我们发现，虽然运动协调和奖励学习在很大程度上没有变化，但这些动物在与努力相关的行为任务中表现出明显的缺陷。这些结果提供了遗传学证据，表明多巴胺能神经元的多巴胺能传递是激励动机的基础，愿意付出高水平的努力来获得多巴胺，并对理解中脑多巴胺系统的正常功能具有重要意义。
Midbrain dopamine neurons are crucial for many behavioral and cognitive functions. As the major excitatory input, glutamatergic afferents are important for control of the activity and plasticity of dopamine neurons. However, the role of glutamatergic input as a whole onto dopamine neurons remains unclear. Here we developed a mouse line in which glutamatergic inputs onto dopamine neurons are specifically impaired, and utilized this genetic model to directly test the role of glutamatergic inputs in dopamine-related functions. We found that while motor coordination and reward learning were largely unchanged, these animals showed prominent deficits in effort-related behavioral tasks. These results provide genetic evidence that glutamatergic transmission onto dopaminergic neurons underlies incentive motivation, a willingness to exert high levels of effort to obtain reinforcers, and have important implications for understanding the normal function of the midbrain dopamine system.