1. Neuroscience
Download icon

Two-photon calcium imaging of the medial prefrontal cortex and hippocampus without cortical invasion

  1. Masashi Kondo
  2. Kenta Kobayashi
  3. Masamichi Ohkura
  4. Junichi Nakai
  5. Masanori Matsuzaki  Is a corresponding author
  1. The University of Tokyo, Japan
  2. National Institute for Physiological Sciences, Japan
  3. Saitama University, Japan
Short Report
  • Cited 25
  • Views 9,189
  • Annotations
Cite this article as: eLife 2017;6:e26839 doi: 10.7554/eLife.26839

Abstract

In vivo two-photon calcium imaging currently allows us to observe the activity of multiple neurons up to ~900 µm below the cortical surface without cortical invasion. However, many important brain areas are located deeper than this. Here, we used an 1100 nm laser that underfilled the back aperture of the objective together with red genetically encoded calcium indicators to establish two-photon calcium imaging of the intact mouse brain and detect neural activity up to 1200 μm from the cortical surface. This imaging was obtained from the medial prefrontal cortex (the prelimbic area) and the hippocampal CA1 region. We found that neural activity before water delivery repeated at a constant interval was higher in the prelimbic area than in layer 2/3 of the secondary motor area. Reducing the invasiveness of imaging is an important strategy to reveal the intact brain processes active in cognition and memory.

Article and author information

Author details

  1. Masashi Kondo

    Department of Physiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8818-8316
  2. Kenta Kobayashi

    Section of Viral Vector Development, National Institute for Physiological Sciences, Okazaki, Japan
    Competing interests
    The authors declare that no competing interests exist.
  3. Masamichi Ohkura

    Brain Science Institute, Saitama University, Saitama, Japan
    Competing interests
    The authors declare that no competing interests exist.
  4. Junichi Nakai

    Brain Science Institute, Saitama University, Saitama, Japan
    Competing interests
    The authors declare that no competing interests exist.
  5. Masanori Matsuzaki

    Department of Physiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
    For correspondence
    mzakim@m.u-tokyo.ac.jp
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-3872-4322

Funding

Ministry of Education, Culture, Sports, Science, and Technology (Grant-in-Aids for Scientific Research on Innovative Areas (15H01455))

  • Masanori Matsuzaki

Ministry of Education, Culture, Sports, Science, and Technology (Grant-in-Aids for Scientific Research on Innovative Areas (17H06309))

  • Masanori Matsuzaki

Ministry of Education, Culture, Sports, Science, and Technology (Grant-in-Aids for Scientific Research (A) (15H02350))

  • Masanori Matsuzaki

Takeda Science Foundation

  • Masanori Matsuzaki

Japan Agency for Medical Research and Development (The Strategic Research Program for Brain Sciences)

  • Masanori Matsuzaki

Japan Agency for Medical Research and Development (The program for Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain/MINDS))

  • Masanori Matsuzaki

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 experiments were approved by the Institutional Animal Care and Use Committee of The University of Tokyo, Japan (Medicine-P16-012).

Reviewing Editor

  1. David Kleinfeld, University of California, San Diego, United States

Publication history

  1. Received: March 15, 2017
  2. Accepted: September 25, 2017
  3. Accepted Manuscript published: September 25, 2017 (version 1)
  4. Version of Record published: October 16, 2017 (version 2)

Copyright

© 2017, Kondo 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

  • 9,189
    Page views
  • 1,498
    Downloads
  • 25
    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. Computational and Systems Biology
    2. Neuroscience
    Tuomo Mäki-Marttunen et al.
    Research Article Updated

    Signalling pathways leading to post-synaptic plasticity have been examined in many types of experimental studies, but a unified picture on how multiple biochemical pathways collectively shape neocortical plasticity is missing. We built a biochemically detailed model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic potentiation or depression. We developed a statistical AMPA-receptor-tetramer model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR2s predicted by the biochemical signalling model. We show that our model reproduces neuromodulator-gated spike-timing-dependent plasticity as observed in the visual cortex and can be fit to data from many cortical areas, uncovering the biochemical contributions of the pathways pinpointed by the underlying experimental studies. Our model explains the dependence of different forms of plasticity on the availability of different proteins and can be used for the study of mental disorder-associated impairments of cortical plasticity.

    1. Neuroscience
    Kazuki Shiotani et al.
    Research Article Updated

    The ventral tenia tecta (vTT) is a component of the olfactory cortex and receives both bottom-up odor signals and top-down signals. However, the roles of the vTT in odor-coding and integration of inputs are poorly understood. Here, we investigated the involvement of the vTT in these processes by recording the activity from individual vTT neurons during the performance of learned odor-guided reward-directed tasks in mice. We report that individual vTT cells are highly tuned to a specific behavioral epoch of learned tasks, whereby the duration of increased firing correlated with the temporal length of the behavioral epoch. The peak time for increased firing among recorded vTT cells encompassed almost the entire temporal window of the tasks. Collectively, our results indicate that vTT cells are selectively activated during a specific behavioral context and that the function of the vTT changes dynamically in a context-dependent manner during goal-directed behaviors.