1. Neuroscience
Download icon

An arbitrary-spectrum spatial visual stimulator for vision research

  1. Katrin Franke
  2. André Maia Chagas
  3. Zhijian Zhao
  4. Maxime JY Zimmermann
  5. Philipp Bartel
  6. Yongrong Qiu
  7. Klaudia P Szatko
  8. Tom Baden
  9. Thomas Euler  Is a corresponding author
  1. University of Tübingen, Germany
  2. University of Sussex, United Kingdom
Tools and Resources
  • Cited 8
  • Views 1,894
  • Annotations
Cite this article as: eLife 2019;8:e48779 doi: 10.7554/eLife.48779

Abstract

Visual neuroscientists require accurate control of visual stimulation. However, few stimulator solutions simultaneously offer high spatio-temporal resolution and free control over the spectra of the light sources, because they rely on off-the-shelf technology developed for human trichromatic vision. Importantly, consumer displays fail to drive UV-shifted short wavelength-sensitive photoreceptors, which strongly contribute to visual behaviour in many animals, including mice, zebrafish and fruit flies. Moreover, many non-mammalian species feature more than three spectral photoreceptor types. Here, we present a flexible, spatial visual stimulator with up to 6 arbitrary spectrum chromatic channels. It combines a standard digital light processing engine with open source hard- and software that can be easily adapted to the experimentalist's needs. We demonstrate the capability of this general visual stimulator experimentally in the in vitro mouse retinal whole-mount and the in vivo zebrafish. With this work, we intend to start a community effort of sharing and developing a common stimulator design for vision research.

Article and author information

Author details

  1. Katrin Franke

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  2. André Maia Chagas

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  3. Zhijian Zhao

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-3302-1495
  4. Maxime JY Zimmermann

    School of Life Sciences, University of Sussex, Brighton, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Philipp Bartel

    School of Life Sciences, University of Sussex, Brighton, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  6. Yongrong Qiu

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  7. Klaudia P Szatko

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  8. Tom Baden

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  9. Thomas Euler

    Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany
    For correspondence
    thomas.euler@cin.uni-tuebingen.de
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-4567-6966

Funding

Bundesministerium für Bildung und Forschung (FKZ: 01GQ1002)

  • Katrin Franke

Max-Planck-Gesellschaft (M.FE.A.KYBE0004)

  • Katrin Franke

European Commission (ERC-StG 'NeuroVisEco' 677687)

  • Tom Baden

Horizon 2020 Framework Programme (Marie Skłodowska-Curie grant agreement No 674901)

  • Tom Baden
  • Thomas Euler

Biotechnology and Biological Sciences Research Council (BB/R014817/1)

  • Tom Baden

Leverhulme Trust (PLP-2017-005)

  • Tom Baden

Lister Institute of Preventive Medicine

  • Tom Baden

Deutsche Forschungsgemeinschaft (Projektnummer 276693517 - SFB 1233)

  • Thomas Euler

Medical Research Council (MC_PC_15071)

  • Tom Baden

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

Ethics

Animal experimentation: All animal procedures adhered to the laws governing animal experimentation issued by the GermanGovernment (mouse) or all procedures were performed in accordance with the UK Animals (ScientificProcedures) act 1986 and approved by the animal welfare committee of the University of Sussex(zebrafish larvae).

Reviewing Editor

  1. Alexander Borst, Max Planck Institute of Neurobiology, Germany

Publication history

  1. Received: May 24, 2019
  2. Accepted: September 20, 2019
  3. Accepted Manuscript published: September 23, 2019 (version 1)
  4. Version of Record published: October 8, 2019 (version 2)

Copyright

© 2019, Franke 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

  • 1,894
    Page views
  • 306
    Downloads
  • 8
    Citations

Article citation count generated by polling the highest count across the following sources: Crossref, Scopus, 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)

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

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

Further reading

    1. Neuroscience
    Junpei Yamashita et al.
    Research Article

    Recent studies in mice demonstrate that a subset of neurons in the medial preoptic area (MPOA) that express galanin play crucial roles in regulating parental behavior in both sexes. However, little information is available on the function of galanin in social behaviors in other species. Here, we report that, in medaka, a subset of MPOA galanin neurons occurred nearly exclusively in males, resulting from testicular androgen stimulation. Galanin-deficient medaka showed a greatly reduced incidence of male–male aggressive chases. Furthermore, while treatment of female medaka with androgen induced male-typical aggressive acts, galanin deficiency in these females attenuated the effect of androgen on chases. Given their male-biased and androgen-dependent nature, the subset of MPOA galanin neurons most likely mediate androgen-dependent male–male chases. Histological studies further suggested that variability in the projection targets of the MPOA galanin neurons may account for the species-dependent functional differences in these evolutionarily conserved neural substrates.

    1. Neuroscience
    Javier Zorrilla de San Martin et al.
    Research Article

    Down syndrome (DS) results in various degrees of cognitive deficits. In DS mouse models, recovery of behavioral and neurophysiological deficits using GABAAR antagonists led to hypothesize an excessive activity of inhibitory circuits in this condition. Nonetheless, whether over-inhibition is present in DS and whether this is due to specific alterations of distinct GABAergic circuits is unknown. In the prefrontal cortex of Ts65Dn mice (a well-established DS model), we found that the dendritic synaptic inhibitory loop formed by somatostatin-positive Martinotti cells (MCs) and pyramidal neurons (PNs) was strongly enhanced, with no alteration in their excitability. Conversely, perisomatic inhibition from parvalbumin-positive (PV) interneurons was unaltered, but PV cells of DS mice lost their classical fast-spiking phenotype and exhibited increased excitability. These microcircuit alterations resulted in reduced pyramidal-neuron firing and increased phase locking to cognitive-relevant network oscillations in vivo. These results define important synaptic and circuit mechanisms underlying cognitive dysfunctions in DS.