Genetic inhibition of neurotransmission reveals role of glutamatergic input to dopamine neurons in high-effort behavior. Mol Psychiatry 2018 May;23(5):1213-1225
Date
02/15/2017Pubmed ID
28194005Pubmed Central ID
PMC5555825DOI
10.1038/mp.2017.7Scopus ID
2-s2.0-85012250772 (requires institutional sign-in at Scopus site) 11 CitationsAbstract
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.
Author List
Hutchison MA, Gu X, Adrover MF, Lee MR, Hnasko TS, Alvarez VA, Lu WAuthor
Ryan M. Lee MD Instructor in the Neurology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsDopamine
Dopaminergic Neurons
Excitatory Amino Acid Agents
Learning
Male
Mesencephalon
Mice
Mice, Transgenic
Motivation
Reward
Synaptic Transmission
