Evidence map›Paper›PMID 32988455›Full record

ArticleeLife2020

A circuit mechanism for decision-making biases and NMDA receptor hypofunction.

Sean Edward Cavanagh, Norman H Lam, John D Murray, Laurence Tudor Hunt, Steven Wayne Kennerley

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Habenula-ventral tegmental area functional coupling and risk aversion in humans.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Effects of Ketamine on Frontoparietal Interactions in a Rule-Based Antisaccade Task in Macaque Monkeys.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Decision-Making, Pro-variance Biases and Mood-Related Traits.Computational psychiatry (Cambridge, Mass.) · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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

5 authors at 3 institutions in 2 countries.

Sean Edward Cavanagh *Department of Clinical and Movement Neurosciences, University College London, London, United Kingdom.ORCID https://orcid.org/0000-0001-9275-2725
Norman H Lam *Department of Physics, Yale University, New Haven, United States.ORCID https://orcid.org/0000-0001-5817-6680
John D Murray *Department of Psychiatry, Yale University School of Medicine, New Haven, United States.ORCID https://orcid.org/0000-0003-4115-8181
Laurence Tudor Hunt *Department of Clinical and Movement Neurosciences, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-8393-8533
Steven Wayne Kennerley *Department of Clinical and Movement Neurosciences, University College London, London, United Kingdom.ORCID https://orcid.org/0000-0002-5696-7507
University College London · GBYale University · USWellcome Centre for Human Neuroimaging · GB

Funding

Linking Large-Scale Dysconnectivity in Schizophrenia to Cortical Circuit Function at the Individual Level through Computational Modeling and Multimodal NeuroimagingR01MH112746 · NIMH · YALE UNIVERSITY · PI MURRAY, JOHN DAVID · 2017 to 2020
$1.7M
NIMH NIH HHS R01 MH112746Wellcome Trust 208789/Z/17/Z
6 · The paper itself

Abstract

Decision-making biases can be features of normal behaviour, or deficits underlying neuropsychiatric symptoms. We used behavioural psychophysics, spiking-circuit modelling and pharmacological manipulations to explore decision-making biases during evidence integration. Monkeys showed a pro-variance bias (PVB): a preference to choose options with more variable evidence. The PVB was also present in a spiking circuit model, revealing a potential neural mechanism for this behaviour. To model possible effects of NMDA receptor (NMDA-R) antagonism on this behaviour, we simulated the effects of NMDA-R hypofunction onto either excitatory or inhibitory neurons in the model. These were then tested experimentally using the NMDA-R antagonist ketamine, a pharmacological model of schizophrenia. Ketamine yielded an increase in subjects' PVB, consistent with lowered cortical excitation/inhibition balance from NMDA-R hypofunction predominantly onto excitatory neurons. These results provide a circuit-level mechanism that bridges across explanatory scales, from the synaptic to the behavioural, in neuropsychiatric disorders where decision-making biases are prominent.

Indexed as

Models, NeurologicalReceptors, N-Methyl-D-AspartateAnimalsBehavior, AnimalChoice BehaviorDecision MakingDisease Models, AnimalExcitatory Amino Acid AntagonistsKetamineMacaca mulattaMalePsychophysicsSchizophreniaExcitatory Amino Acid AntagonistsKetamineReceptors, N-Methyl-D-Aspartatedecision-makingketaminenetwork modelneuroscienceNMDA receptorrhesus macaqueschizophrenia

Identifiers

PMID32988455
PMCPMC7524553
OpenAlexW3091581001

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.