Evidence map›Paper›PMID 18815248›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Tripartite mechanism of extinction suggested by dopamine neuron activity and temporal difference model.

Wei-Xing Pan, Robert Schmidt, Jeffery R Wickens, Brian I Hyland

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed.

  1. KChIP4a is a Biophysical Amplifier of Inhibition in Atypical Dopamine Neurons and Controls Learning from Negative Prediction Errors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  2. Article
  3. Article
  4. Natural phasic inhibition of dopamine neurons signals cognitive rigidity.bioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Neurons of the Ventral Tegmental Area Encode Individual Differences in Motivational "Wanting" for Reward Cues.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  7. Article
  8. Abundance Compensates Kinetics: Similar Effect of Dopamine Signals on D1 and D2 Receptor Populations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Model-based predictions for dopamine.Current opinion in neurobiology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. A Specific Component of the Evoked Potential Mirrors Phasic Dopamine Neuron Activity during Conditioning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  19. Actigraph evaluation of acupuncture for treating restless legs syndrome.Evidence-based complementary and alternative medicine : eCAM · 2015
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Wei-Xing PanDepartment of Physiology, School of Medical Sciences, University of Otago, Dunedin 9054, New Zealand.
Robert Schmidt
Jeffery R Wickens
Brian I Hyland

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extinction of behavior enables adaptation to a changing world and is crucial for recovery from disorders such as phobias and drug addiction. However, the brain mechanisms underlying behavioral extinction remain poorly understood. Midbrain dopamine (DA) neurons appear to play a central role in most acquisition processes of appetitive conditioning. Here, we show that the responses of putative DA neurons to conditioned reward predicting cues also dynamically encode two classical features of extinction: decrement in amplitude of previously learned excitatory responses and rebound of responding on subsequent retesting (spontaneous recovery). Crucially, this encoding involves development of inhibitory responses in the DA neurons, reflecting new, extinction-specific learning in the brain. We explored the implications of this finding by adding such inhibitory inputs to a standard temporal difference model of DA cell activity. We found that combining extinction-triggered plasticity of these inputs with a time-dependent spontaneous decay of weights, equivalent to a forgetting process as described in classical behavioral extinction literature, enabled the model to simulate several classical features of extinction. A key requirement to achieving spontaneous recovery was differential rates of spontaneous decay for weights representing original conditioning and for subsequent extinction learning. A testable prediction of the model is thus that differential decay properties exist within the wider circuits regulating DA cell activity. These findings are consistent with the hypothesis that extinction processes at both cellular and behavioral levels involve a dynamic interaction between new (inhibitory) learning, forgetting, and unlearning.

Indexed as

Models, NeurologicalAcoustic StimulationAction PotentialsAlgorithmsAnimalsBehavior, AnimalBicucullineConditioning, PsychologicalCuesDopamineExtinction, PsychologicalGABA AntagonistsMaleNeuronsRatsRats, WistarBicucullineDopamineGABA Antagonists

Identifiers

PMID18815248
PMCPMC6671219

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.