Causal links between parietal alpha activity and spatial auditory attention

  1. Yuqi Deng
  2. Robert MG Reinhart
  3. Inyong Choi
  4. Barbara G Shinn-Cunningham  Is a corresponding author
  1. Boston University, United States
  2. University of Iowa, United States
  3. Carnegie Mellon University, United States


Both visual and auditory spatial selective attention result in lateralized alpha (8-14 Hz) oscillatory power in parietal cortex: alpha increases in the hemisphere ipsilateral to attentional focus. Brain stimulation studies suggest a causal relationship between parietal alpha and suppression of the representation of contralateral visual space. However, there is no evidence that parietal alpha controls auditory spatial attention. Here, we performed high definition transcranial alternating current stimulation (HD-tACS) on human subjects performing an auditory task in which they directed attention based on either spatial or nonspatial features. Alpha (10 Hz) but not theta (6 Hz) HD-tACS of right parietal cortex interfered with attending left but not right auditory space. Parietal stimulation had no effect for nonspatial auditory attention. Moreover, performance in post-stimulation trials returned rapidly to baseline. These results demonstrate a causal, frequency-, hemispheric-, and task-specific effect of parietal alpha brain stimulation on top-down control of auditory spatial attention.

Data availability

Data are available from Dryad at

The following data sets were generated

Article and author information

Author details

  1. Yuqi Deng

    Biomedical Engineering, Boston University, Boston, United States
    Competing interests
    No competing interests declared.
  2. Robert MG Reinhart

    Psychological and Brain Sciences, Boston University, Boston, United States
    Competing interests
    No competing interests declared.
  3. Inyong Choi

    Communication Sciences and Disorders, University of Iowa, Iowa, United States
    Competing interests
    No competing interests declared.
  4. Barbara G Shinn-Cunningham

    Carnegie Mellon Neuroscience Institute, Carnegie Mellon University, Pittsburgh, United States
    For correspondence
    Competing interests
    Barbara G Shinn-Cunningham, Senior editor, eLife.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-5096-5914


National Institutes of Health (R01 DC015988)

  • Barbara G Shinn-Cunningham

Office of Naval Research (N000141812069)

  • Barbara G Shinn-Cunningham

National Institutes of Health (R01 MH-114877)

  • Robert MG Reinhart

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


Human subjects: All subjects gave informed consent, as approved by the Boston University Charles River Campus IRB, under protocol 3597E.

Reviewing Editor

  1. Huan Luo, Peking University, China

Publication history

  1. Received: August 19, 2019
  2. Accepted: November 28, 2019
  3. Accepted Manuscript published: November 29, 2019 (version 1)
  4. Version of Record published: December 10, 2019 (version 2)


© 2019, Deng 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.


  • 1,626
    Page views
  • 242
  • 24

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)

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. Yuqi Deng
  2. Robert MG Reinhart
  3. Inyong Choi
  4. Barbara G Shinn-Cunningham
Causal links between parietal alpha activity and spatial auditory attention
eLife 8:e51184.
  1. Further reading

Further reading

    1. Developmental Biology
    2. Neuroscience
    Anadika R Prasad, Inês Lago-Baldaia ... Vilaiwan M Fernandes
    Research Article Updated

    Neural circuit formation and function require that diverse neurons are specified in appropriate numbers. Known strategies for controlling neuronal numbers involve regulating either cell proliferation or survival. We used the Drosophila visual system to probe how neuronal numbers are set. Photoreceptors from the eye-disc induce their target field, the lamina, such that for every unit eye there is a corresponding lamina unit (column). Although each column initially contains ~6 post-mitotic lamina precursors, only 5 differentiate into neurons, called L1-L5; the ‘extra’ precursor, which is invariantly positioned above the L5 neuron in each column, undergoes apoptosis. Here, we showed that a glial population called the outer chiasm giant glia (xgO), which resides below the lamina, secretes multiple ligands to induce L5 differentiation in response to epidermal growth factor (EGF) from photoreceptors. By forcing neuronal differentiation in the lamina, we uncovered that though fated to die, the ‘extra’ precursor is specified as an L5. Therefore, two precursors are specified as L5s but only one differentiates during normal development. We found that the row of precursors nearest to xgO differentiate into L5s and, in turn, antagonise differentiation signalling to prevent the ‘extra’ precursors from differentiating, resulting in their death. Thus, an intricate interplay of glial signals and feedback from differentiating neurons defines an invariant and stereotyped pattern of neuronal differentiation and programmed cell death to ensure that lamina columns each contain exactly one L5 neuron.

    1. Neuroscience
    Brittany J Bush, Caroline Donnay ... J Christopher Ehlen
    Research Article

    Resilience, the ability to overcome stressful conditions, is found in most mammals and varies significantly among individuals. A lack of resilience can lead to the development of neuropsychiatric and sleep disorders, often within the same individual. Despite extensive research into the brain mechanisms causing maladaptive behavioral-responses to stress, it is not clear why some individuals exhibit resilience. To examine if sleep has a determinative role in maladaptive behavioral-response to social stress, we investigated individual variations in resilience using a social-defeat model for male mice. Our results reveal a direct, causal relationship between sleep amount and resilience-demonstrating that sleep increases after social-defeat stress only occur in resilient mice. Further, we found that within the prefrontal cortex, a regulator of maladaptive responses to stress, pre-existing differences in sleep regulation predict resilience. Overall, these results demonstrate that increased NREM sleep, mediated cortically, is an active response to social-defeat stress that plays a determinative role in promoting resilience. They also show that differences in resilience are strongly correlated with inter-individual variability in sleep regulation.