Differentiating between integration and non-integration strategies in perceptual decision making

  1. Gabriel M Stine  Is a corresponding author
  2. Ariel Zylberberg
  3. Jochen Ditterich
  4. Michael N Shadlen
  1. Columbia University, United States
  2. University of Rochester, United States
  3. University of California, Davis, United States

Abstract

Many tasks used to study decision-making encourage subjects to integrate evidence over time. Such tasks are useful to understand how the brain operates on multiple samples of information over prolonged timescales, but only if subjects actually integrate evidence to form their decisions. We explored the behavioral observations that corroborate evidence-integration in a number of task-designs. Several commonly accepted signs of integration were also predicted by non-integration strategies. Furthermore, an integration model could fit data generated by non-integration models. We identified the features of non-integration models that allowed them to mimic integration and used these insights to design a motion discrimination task that disentangled the models. In human subjects performing the task, we falsified a non-integration strategy in each and confirmed prolonged integration in all but one subject. The findings illustrate the difficulty of identifying a decision-maker's strategy and support solutions to achieve this goal.

Data availability

The data generated during this study are included in the source data file for Figure 6.

Article and author information

Author details

  1. Gabriel M Stine

    Neuroscience, Columbia University, New York, United States
    For correspondence
    gabriel.stine@columbia.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-4906-0461
  2. Ariel Zylberberg

    Brain and Cognitive Sciences, University of Rochester, Rochester, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2572-4748
  3. Jochen Ditterich

    Center for Neuroscience, University of California, Davis, Davis, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Michael N Shadlen

    Department of Neuroscience, Columbia University, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2002-2210

Funding

Howard Hughes Medical Institute

  • Ariel Zylberberg
  • Michael N Shadlen

National Eye Institute (EY011378)

  • Gabriel M Stine
  • Ariel Zylberberg
  • Michael N Shadlen

National Eye Institute (EY013933)

  • Gabriel M Stine

National Institute of Neurological Disorders and Stroke (NS113113)

  • Gabriel M Stine
  • Ariel Zylberberg
  • Michael N Shadlen

Israel Institute for Advanced Studies

  • Michael N Shadlen

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Human subjects: Human subjects: The institutional review board of Columbia University (protocol #IRB-AAAL0658) approved the experimental protocol, and subjects gave written informed consent.

Reviewing Editor

  1. Valentin Wyart, École normale supérieure, PSL University, INSERM, France

Version history

  1. Received: January 21, 2020
  2. Accepted: April 24, 2020
  3. Accepted Manuscript published: April 27, 2020 (version 1)
  4. Version of Record published: May 12, 2020 (version 2)

Copyright

© 2020, Stine et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 5,297
    Page views
  • 736
    Downloads
  • 33
    Citations

Article citation count generated by polling the highest count across the following sources: Scopus, Crossref, PubMed Central.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Gabriel M Stine
  2. Ariel Zylberberg
  3. Jochen Ditterich
  4. Michael N Shadlen
(2020)
Differentiating between integration and non-integration strategies in perceptual decision making
eLife 9:e55365.
https://doi.org/10.7554/eLife.55365

Further reading

    1. Genetics and Genomics
    2. Neuroscience
    Yoshifumi Sonobe, Soojin Lee ... Paschalis Kratsios
    Research Article Updated

    A hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A hallmark of ALS/FTD pathology is the presence of dipeptide repeat (DPR) proteins, produced from both sense GGGGCC (poly-GA, poly-GP, poly-GR) and antisense CCCCGG (poly-PR, poly-PG, poly-PA) transcripts. Translation of sense DPRs, such as poly-GA and poly-GR, depends on non-canonical (non-AUG) initiation codons. Here, we provide evidence for canonical AUG-dependent translation of two antisense DPRs, poly-PR and poly-PG. A single AUG is required for synthesis of poly-PR, one of the most toxic DPRs. Unexpectedly, we found redundancy between three AUG codons necessary for poly-PG translation. Further, the eukaryotic translation initiation factor 2D (EIF2D), which was previously implicated in sense DPR synthesis, is not required for AUG-dependent poly-PR or poly-PG translation, suggesting that distinct translation initiation factors control DPR synthesis from sense and antisense transcripts. Our findings on DPR synthesis from the C9ORF72 locus may be broadly applicable to many other nucleotide repeat expansion disorders.

    1. Cell Biology
    2. Neuroscience
    Elisabeth Jongsma, Anita Goyala ... Collin Yvès Ewald
    Research Article Updated

    The amyloid beta (Aβ) plaques found in Alzheimer’s disease (AD) patients’ brains contain collagens and are embedded extracellularly. Several collagens have been proposed to influence Aβ aggregate formation, yet their role in clearance is unknown. To investigate the potential role of collagens in forming and clearance of extracellular aggregates in vivo, we created a transgenic Caenorhabditis elegans strain that expresses and secretes human Aβ1-42. This secreted Aβ forms aggregates in two distinct places within the extracellular matrix. In a screen for extracellular human Aβ aggregation regulators, we identified different collagens to ameliorate or potentiate Aβ aggregation. We show that a disintegrin and metalloprotease a disintegrin and metalloprotease 2 (ADM-2), an ortholog of ADAM9, reduces the load of extracellular Aβ aggregates. ADM-2 is required and sufficient to remove the extracellular Aβ aggregates. Thus, we provide in vivo evidence of collagens essential for aggregate formation and metalloprotease participating in extracellular Aβ aggregate removal.