1. Neuroscience
Download icon

Bottom-up and top-down influences at untrained conditions determine perceptual learning specificity and transfer

  1. Ying-Zi Xiong
  2. Jun-Yun Zhang
  3. Cong Yu  Is a corresponding author
  1. Peking University, China
Research Article
  • Cited 21
  • Views 1,629
  • Annotations
Cite this article as: eLife 2016;5:e14614 doi: 10.7554/eLife.14614


Perceptual learning is often orientation and location specific, which may indicate neuronal plasticity in early visual areas. However, learning specificity diminishes with additional exposure of the transfer orientation or location via irrelevant tasks, suggesting that the specificity is related to untrained conditions, likely because neurons representing untrained conditions are neither bottom-up stimulated nor top-down attended during training. To demonstrate these top-down and bottom-up contributions, we applied a 'continuous flash suppression' technique to suppress the exposure stimulus into sub-consciousness, and with additional manipulations to achieve pure bottom-up stimulation or top-down attention with the transfer condition. We found that either bottom-up or top-down influences enabled significant transfer of orientation and Vernier discrimination learning. These results suggest that learning specificity may result from under-activations of untrained visual neurons due to insufficient bottom-up stimulation and/or top-down attention during training. High-level perceptual learning thus may not functionally connect to these neurons for learning transfer.

Article and author information

Author details

  1. Ying-Zi Xiong

    School of Psychological and Cognitive Sciences, Peking University, Beijing, China
    Competing interests
    The authors declare that no competing interests exist.
  2. Jun-Yun Zhang

    School of Psychological and Cognitive Sciences, Peking University, Beijing, China
    Competing interests
    The authors declare that no competing interests exist.
  3. Cong Yu

    School of Psychological and Cognitive Sciences, Peking University, Beijing, China
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-8453-6974


Human subjects: Informed consent, and consent to publish was obtained from each observer before testing. This study was approved by the Peking University Institution Review Board.

Reviewing Editor

  1. Joshua I Gold, University of Pennsylvania, United States

Publication history

  1. Received: January 21, 2016
  2. Accepted: July 4, 2016
  3. Accepted Manuscript published: July 5, 2016 (version 1)
  4. Version of Record published: July 28, 2016 (version 2)
  5. Version of Record updated: August 18, 2016 (version 3)


© 2016, Xiong 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.


  • 1,629
    Page views
  • 307
  • 21

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)

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. Cell Biology
    2. Neuroscience
    Domenica Ippolito et al.
    Research Article Updated

    Sensory and behavioral plasticity are essential for animals to thrive in changing environments. As key effectors of intracellular calcium signaling, Ca2+/calmodulin-dependent protein kinases (CaMKs) can bridge neural activation with the many regulatory processes needed to orchestrate sensory adaptation, including by relaying signals to the nucleus. Here, we elucidate the molecular mechanism controlling the cell activation-dependent nuclear translocation of CMK-1, the Caenorhabditis elegans ortholog of mammalian CaMKI/IV, in thermosensory neurons in vivo. We show that an intracellular Ca2+ concentration elevation is necessary and sufficient to favor CMK-1 nuclear import. The binding of Ca2+/CaM to CMK-1 increases its affinity for IMA-3 importin, causing a redistribution with a relatively slow kinetics, matching the timescale of sensory adaptation. Furthermore, we show that this mechanism enables the encoding of opposite nuclear signals in neuron types with opposite calcium-responses and that it is essential for experience-dependent behavioral plasticity and gene transcription control in vivo. Since CaMKI/IV are conserved regulators of adaptable behaviors, similar mechanisms could exist in other organisms and for other sensory modalities.