1. Neuroscience

MouseBytes, an open-access high-throughput pipeline and database for rodent touchscreen-based cognitive assessment

  1. Flavio H Beraldo
  2. Daniel Palmer
  3. Sara Memar
  4. David I Wasserman
  5. Wai-Jane V Lee
  6. Shuai Liang
  7. Samantha D Creighton
  8. Benjamin Kolisnyk
  9. Matthew F Cowan
  10. Justin Mels
  11. Talal S Masood
  12. Chris Fodor
  13. Mohammed A Al-Onaizi
  14. Robert Bartha
  15. Tom Gee
  16. Lisa M Saksida
  17. Timothy J Bussey
  18. Stephen S Strother
  19. Vania F Prado
  20. Boyer D Winters  Is a corresponding author
  21. Marco A M Prado  Is a corresponding author
  1. University of Western Ontario, Canada
  2. Rotman Research Institute, Baycrest Hospital, Canada
  3. University of Guelph, Canada
https://doi.org/10.7554/eLife.49630
Share this article
Cite this article
  1. Flavio H Beraldo
  2. Daniel Palmer
  3. Sara Memar
  4. David I Wasserman
  5. Wai-Jane V Lee
  6. Shuai Liang
  7. Samantha D Creighton
  8. Benjamin Kolisnyk
  9. Matthew F Cowan
  10. Justin Mels
  11. Talal S Masood
  12. Chris Fodor
  13. Mohammed A Al-Onaizi
  14. Robert Bartha
  15. Tom Gee
  16. Lisa M Saksida
  17. Timothy J Bussey
  18. Stephen S Strother
  19. Vania F Prado
  20. Boyer D Winters
  21. Marco A M Prado
(2019)
MouseBytes, an open-access high-throughput pipeline and database for rodent touchscreen-based cognitive assessment
eLife 8:e49630.
https://doi.org/10.7554/eLife.49630
  2. Download BibTeX
  3. Download .RIS

Abstract

Open Science has changed research by making data accessible and shareable, contributing to replicability to accelerate and disseminate knowledge. However, for rodent cognitive studies the availability of tools to share and disseminate data is scarce. Automated touchscreen-based tests enable systematic cognitive assessment with easily standardized outputs that can facilitate data dissemination. Here we present an integration of touchscreen cognitive testing with an open-access database public repository (mousebytes.ca), as well as a Web platform for knowledge dissemination (https://touchscreencognition.org). We complement these resources with the largest dataset of age-dependent high-level cognitive assessment of mouse models of Alzheimer's disease, expanding knowledge of affected cognitive domains from male and female mice of three mouse strains. We envision that these new platforms will enhance sharing of protocols, data availability and transparency, allowing meta-analysis and reuse of mouse cognitive data to increase the replicability/reproducibility of datasets.

Data availability

Automated quality control (QC) algorithm and the codes are available for free download and modification in GitHub https://github.com/srmemar/Mousebytes-An-open-access-high-throughput-pipeline-and-database-for-rodent-touchscreen-based-dataThe touchscreen processed data were deposited into an open-access application (http://www.mousebytes.ca/).

Article and author information

Author details

  1. Flavio H Beraldo

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  2. Daniel Palmer

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  3. Sara Memar

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  4. David I Wasserman

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  5. Wai-Jane V Lee

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  6. Shuai Liang

    Rotman Research Institute, Baycrest Hospital, Toronto, Canada
    Competing interests
    No competing interests declared.

  7. Samantha D Creighton

    Department of Psychology and Neuroscience Program, University of Guelph, Guelph, Canada
    Competing interests
    No competing interests declared.

  8. Benjamin Kolisnyk

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  9. Matthew F Cowan

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  10. Justin Mels

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  11. Talal S Masood

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  12. Chris Fodor

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  13. Mohammed A Al-Onaizi

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  14. Robert Bartha

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  15. Tom Gee

    Rotman Research Institute, Baycrest Hospital, Toronto, Canada
    Competing interests
    No competing interests declared.

  16. Lisa M Saksida

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    Lisa M Saksida, consults for Campden Instruments, Ltd.

  17. Timothy J Bussey

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    Timothy J Bussey, consults for Campden Instruments, Ltd.

  18. Stephen S Strother

    Rotman Research Institute, Baycrest Hospital, Toronto, Canada
    Competing interests
    No competing interests declared.

  19. Vania F Prado

    Robarts Research Institute, University of Western Ontario, London, Canada
    Competing interests
    No competing interests declared.

  20. Boyer D Winters

    Department of Psychology and Neuroscience Program, University of Guelph, Guelph, Canada
    For correspondence
    bwinters@uoguelph.ca
    Competing interests
    No competing interests declared.

  21. Marco A M Prado

    Robarts Research Institute, University of Western Ontario, London, Canada
    For correspondence
    mprado@robarts.ca
    Competing interests
    No competing interests declared.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-3028-5778

Funding

Weston Brain Institute

  • Robert Bartha
  • Stephen S Strother
  • Boyer D Winters
  • Marco A M Prado

Canada Open Neuroscience Platform

  • Sara Memar
  • Timothy J Bussey
  • Marco A M Prado

Mitacs

  • Daniel Palmer
  • Lisa M Saksida
  • Timothy J Bussey

CIFAR

  • Lisa M Saksida

Canadian Institutes of Health Research (MOP136930)

  • Marco A M Prado

Alzheimer's Society

  • Vania F Prado
  • Marco A M Prado

Canada First Research Excellence Fund (BrainsCAN)

  • Robert Bartha
  • Lisa M Saksida
  • Timothy J Bussey
  • Vania F Prado
  • Marco A M Prado

Brain Canada

  • Vania F Prado
  • Marco A M Prado

Canadian Institutes of Health Research (MOP126000)

  • Vania F Prado
  • Marco A M Prado

Canadian Institutes of Health Research (MOP89919)

  • Vania F Prado
  • Marco A M Prado

Natural Sciences and Engineering Research Council of Canada

  • Lisa M Saksida
  • Timothy J Bussey
  • Vania F Prado

Canada Research Chairs

  • Lisa M Saksida
  • Marco A M Prado

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

Ethics

Animal experimentation: Procedures were conducted in accordance with approved animal protocols at the University of Western Ontario (2016/104) and the University of Guelph (3481) following the Canadian Council of Animal Care and National Institutes of Health guidelines.

Copyright

© 2019, Beraldo 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

  • 3,371
    views
  • 311
    downloads
  • 37
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

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. Flavio H Beraldo
  2. Daniel Palmer
  3. Sara Memar
  4. David I Wasserman
  5. Wai-Jane V Lee
  6. Shuai Liang
  7. Samantha D Creighton
  8. Benjamin Kolisnyk
  9. Matthew F Cowan
  10. Justin Mels
  11. Talal S Masood
  12. Chris Fodor
  13. Mohammed A Al-Onaizi
  14. Robert Bartha
  15. Tom Gee
  16. Lisa M Saksida
  17. Timothy J Bussey
  18. Stephen S Strother
  19. Vania F Prado
  20. Boyer D Winters
  21. Marco A M Prado
(2019)
MouseBytes, an open-access high-throughput pipeline and database for rodent touchscreen-based cognitive assessment
eLife 8:e49630.
https://doi.org/10.7554/eLife.49630

Share this article

https://doi.org/10.7554/eLife.49630

Categories and tags

Research organism

Further reading

    1. Neuroscience

    Parabrachial CGRP neurons modulate active defensive behavior under a naturalistic threat

    Gyeong Hee Pyeon, Hyewon Cho ... Yong Sang Jo
    Research Article Updated

    Recent studies suggest that calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) represent aversive information and signal a general alarm to the forebrain. If CGRP neurons serve as a true general alarm, their activation would modulate both passive nad active defensive behaviors depending on the magnitude and context of the threat. However, most prior research has focused on the role of CGRP neurons in passive freezing responses, with limited exploration of their involvement in active defensive behaviors. To address this, we examined the role of CGRP neurons in active defensive behavior using a predator-like robot programmed to chase mice. Our electrophysiological results revealed that CGRP neurons encode the intensity of aversive stimuli through variations in firing durations and amplitudes. Optogenetic activation of CGRP neurons during robot chasing elevated flight responses in both conditioning and retention tests, presumably by amplifying the perception of the threat as more imminent and dangerous. In contrast, animals with inactivated CGRP neurons exhibited reduced flight responses, even when the robot was programmed to appear highly threatening during conditioning. These findings expand the understanding of CGRP neurons in the PBN as a critical alarm system, capable of dynamically regulating active defensive behaviors by amplifying threat perception, and ensuring adaptive responses to varying levels of danger.

    1. Neuroscience

    Disruption of the CRF1 receptor eliminates morphine-induced sociability deficits and firing of oxytocinergic neurons in male mice

    Alessandro Piccin, Anne-Emilie Allain ... Angelo Contarino
    Research Article

    Substance-induced social behavior deficits dramatically worsen the clinical outcome of substance use disorders; yet, the underlying mechanisms remain poorly understood. Herein, we investigated the role for the corticotropin-releasing factor receptor 1 (CRF1) in the acute sociability deficits induced by morphine and the related activity of oxytocin (OXY)- and arginine-vasopressin (AVP)-expressing neurons of the paraventricular nucleus of the hypothalamus (PVN). For this purpose, we used both the CRF1 receptor-preferring antagonist compound antalarmin and the genetic mouse model of CRF1 receptor-deficiency. Antalarmin completely abolished sociability deficits induced by morphine in male, but not in female, C57BL/6J mice. Accordingly, genetic CRF1 receptor-deficiency eliminated morphine-induced sociability deficits in male mice. Ex vivo electrophysiology studies showed that antalarmin also eliminated morphine-induced firing of PVN neurons in male, but not in female, C57BL/6J mice. Likewise, genetic CRF1 receptor-deficiency reduced morphine-induced firing of PVN neurons in a CRF1 gene expression-dependent manner. The electrophysiology results consistently mirrored the behavioral results, indicating a link between morphine-induced PVN activity and sociability deficits. Interestingly, in male mice antalarmin abolished morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP. In contrast, in female mice antalarmin did not affect morphine-induced firing of neurons co-expressing OXY and AVP or only OXY, indicating a selective sex-specific role for the CRF1 receptor in opiate-induced PVN OXY activity. The present findings demonstrate a major, sex-linked, role for the CRF1 receptor in sociability deficits and related brain alterations induced by morphine, suggesting new therapeutic strategy for opiate use disorders.

    1. Neuroscience

    Cortical tracking of hierarchical rhythms orchestrates the multisensory processing of biological motion

    Li Shen, Shuo Li ... Yi Jiang
    Research Article

    When observing others’ behaviors, we continuously integrate their movements with the corresponding sounds to enhance perception and develop adaptive responses. However, how the human brain integrates these complex audiovisual cues based on their natural temporal correspondence remains unclear. Using electroencephalogram (EEG), we demonstrated that rhythmic cortical activity tracked the hierarchical rhythmic structures in audiovisually congruent human walking movements and footstep sounds. Remarkably, the cortical tracking effects exhibit distinct multisensory integration modes at two temporal scales: an additive mode in a lower-order, narrower temporal integration window (step cycle) and a super-additive enhancement in a higher-order, broader temporal window (gait cycle). Furthermore, while neural responses at the lower-order timescale reflect a domain-general audiovisual integration process, cortical tracking at the higher-order timescale is exclusively engaged in the integration of biological motion cues. In addition, only this higher-order, domain-specific cortical tracking effect correlates with individuals’ autistic traits, highlighting its potential as a neural marker for autism spectrum disorder. These findings unveil the multifaceted mechanism whereby rhythmic cortical activity supports the multisensory integration of human motion, shedding light on how neural coding of hierarchical temporal structures orchestrates the processing of complex, natural stimuli across multiple timescales.