Evidence map›Paper›PMID 29468191›Full record

ArticleeNeuro

A Neural Circuit Mechanism for the Involvements of Dopamine in Effort-Related Choices: Decay of Learned Values, Secondary Effects of Depletion, and Calculation of Temporal Difference Error.

Kenji Morita, Ayaka Kato

Abstract read
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Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Kenji MoritaPhysical and Health Education, Graduate School of Education, the University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0003-2192-4248
Ayaka KatoDepartment of Biological Sciences, Graduate School of Science, the University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0002-6306-6600

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dopamine has been suggested to be crucially involved in effort-related choices. Key findings are that dopamine depletion (i) changed preference for a high-cost, large-reward option to a low-cost, small-reward option, (ii) but not when the large-reward option was also low-cost or the small-reward option gave no reward, (iii) while increasing the latency in all the cases but only transiently, and (iv) that antagonism of either dopamine D1 or D2 receptors also specifically impaired selection of the high-cost, large-reward option. The underlying neural circuit mechanisms remain unclear. Here we show that findings i-iii can be explained by the dopaminergic representation of temporal-difference reward-prediction error (TD-RPE), whose mechanisms have now become clarified, if (1) the synaptic strengths storing the values of actions mildly decay in time and (2) the obtained-reward-representing excitatory input to dopamine neurons increases after dopamine depletion. The former is potentially caused by background neural activity-induced weak synaptic plasticity, and the latter is assumed to occur through post-depletion increase of neural activity in the pedunculopontine nucleus, where neurons representing obtained reward exist and presumably send excitatory projections to dopamine neurons. We further show that finding iv, which is nontrivial given the suggested distinct functions of the D1 and D2 corticostriatal pathways, can also be explained if we additionally assume a proposed mechanism of TD-RPE calculation, in which the D1 and D2 pathways encode the values of actions with a temporal difference. These results suggest a possible circuit mechanism for the involvements of dopamine in effort-related choices and, simultaneously, provide implications for the mechanisms of TD-RPE calculation.

Indexed as

Choice BehaviorMotivationRewardAnimalsComputer SimulationCorpus StriatumDopamineHumansModels, NeurologicalNeuronsReceptors, Dopamine D1Receptors, Dopamine D2DopamineReceptors, Dopamine D1Receptors, Dopamine D2Computational modelingdopamineeffortmotivationreinforcement learningreward prediction error

Identifiers

PMID29468191
PMCPMC5820541

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.