1. Neuroscience
Download icon

Shared neural underpinnings of multisensory integration and trial-by-trial perceptual recalibration in humans

  1. Hame Park  Is a corresponding author
  2. Christoph Kayser  Is a corresponding author
  1. Bielefeld University, Germany
Research Article
  • Cited 14
  • Views 1,663
  • Annotations
Cite this article as: eLife 2019;8:e47001 doi: 10.7554/eLife.47001


Perception adapts to mismatching multisensory information, both when different cues appear simultaneously and when they appear sequentially. While both multisensory integration and adaptive trial-by-trial recalibration are central for behavior, it remains unknown whether they are mechanistically linked and arise from a common neural substrate. To relate the neural underpinnings of sensory integration and recalibration, we measured whole-brain magnetoencephalography while human participants performed an audio-visual ventriloquist task. Using single-trial multivariate analysis, we localized the perceptually-relevant encoding of multisensory information within and between trials. While we found neural signatures of multisensory integration within temporal and parietal regions, only medial superior parietal activity encoded past and current sensory information and mediated the perceptual recalibration within and between trials. These results highlight a common neural substrate of sensory integration and perceptual recalibration, and reveal a role of medial parietal regions in linking present and previous multisensory evidence to guide adaptive behavior.

Data availability

The behavioral data presented in Figure 1 and LDA performance data and source regression data used to calculate the t-values in Figures 2-5, as well as data for Figure 4-figure supplement 1 have been deposited on Dryad (https://dx.doi.org/10.5061/dryad.t0p9c93).

The following data sets were generated

Article and author information

Author details

  1. Hame Park

    Department for Cognitive Neuroscience, Faculty of Biology, Bielefeld University, Bielefeld, Germany
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2191-2055
  2. Christoph Kayser

    Department for Cognitive Neuroscience, Faculty of Biology, Bielefeld University, Bielefeld, Germany
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-7362-5704


H2020 European Research Council (ERC-2014-CoG No 646657)

  • Christoph Kayser

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


Human subjects: All participants submitted written informed consent. The study was conducted in accordance with the Declaration of Helsinki and was approved by the local ethics committee. Ethics Application No: 300140078 (College of Science and Engineering, University of Glasgow).

Reviewing Editor

  1. Ross K Maddox, University of Rochester, United States

Publication history

  1. Received: March 19, 2019
  2. Accepted: June 26, 2019
  3. Accepted Manuscript published: June 27, 2019 (version 1)
  4. Version of Record published: July 26, 2019 (version 2)


© 2019, Park & Kayser

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.


  • 1,663
    Page views
  • 276
  • 14

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

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
    Qing-Tao Meng et al.
    Research Article Updated

    Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCβ-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice.

    1. Cell Biology
    2. Neuroscience
    Sergio Velasco-Aviles et al.
    Research Article

    The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express Hdac4, 5 and 7 but not Hdac9. Here we show that a transcription factor regulated genetic compensatory mechanism within this family of proteins, blocks negative regulators of myelination ensuring peripheral nerve developmental myelination and remyelination after injury. Thus, when Hdac4 and 5 are knocked-out from Schwann cells in mice, a JUN-dependent mechanism induces the compensatory overexpression of Hdac7 permitting, although with a delay, the formation of the myelin sheath. When Hdac4,5 and 7 are simultaneously removed, the Myocyte-specific enhancer-factor d (MEF2D) binds to the promoter and induces the de novo expression of Hdac9, and although several melanocytic lineage genes are misexpressed and Remak bundle structure is disrupted, myelination proceeds after a long delay. Thus, our data unveil a finely tuned compensatory mechanism within the class IIa Hdac family, coordinated by distinct transcription factors, that guarantees the ability of Schwann cells to myelinate during development and remyelinate after nerve injury.