Causal links between parietal alpha activity and spatial auditory attention
- Boston University, United States
- University of Iowa, United States
- Carnegie Mellon University, United States
Abstract
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 https://dx.doi.org/10.5061/dryad.c031nv7
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Data from: Causal links between parietal alpha activity and spatial auditory attentionDryad Digital Repository, doi:10.5061/dryad.c031nv7.
Article and author information
Author details
Barbara G Shinn-Cunningham
Funding
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.
Reviewing Editor
- Huan Luo, Peking University, China
Ethics
Human subjects: All subjects gave informed consent, as approved by the Boston University Charles River Campus IRB, under protocol 3597E.
Version history
- Received: August 19, 2019
- Accepted: November 28, 2019
- Accepted Manuscript published: November 29, 2019 (version 1)
- Version of Record published: December 10, 2019 (version 2)
Copyright
© 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.
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Causal links between parietal alpha activity and spatial auditory attention
eLife 8:e51184.
https://doi.org/10.7554/eLife.51184
Further reading
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- Neuroscience
The presence of global synchronization of vasomotion induced by oscillating visual stimuli was identified in the mouse brain. Endogenous autofluorescence was used and the vessel ‘shadow’ was quantified to evaluate the magnitude of the frequency-locked vasomotion. This method allows vasomotion to be easily quantified in non-transgenic wild-type mice using either the wide-field macro-zoom microscopy or the deep-brain fiber photometry methods. Vertical stripes horizontally oscillating at a low temporal frequency (0.25 Hz) were presented to the awake mouse, and oscillatory vasomotion locked to the temporal frequency of the visual stimulation was induced not only in the primary visual cortex but across a wide surface area of the cortex and the cerebellum. The visually induced vasomotion adapted to a wide range of stimulation parameters. Repeated trials of the visual stimulus presentations resulted in the plastic entrainment of vasomotion. Horizontally oscillating visual stimulus is known to induce horizontal optokinetic response (HOKR). The amplitude of the eye movement is known to increase with repeated training sessions, and the flocculus region of the cerebellum is known to be essential for this learning to occur. Here, we show a strong correlation between the average HOKR performance gain and the vasomotion entrainment magnitude in the cerebellar flocculus. Therefore, the plasticity of vasomotion and neuronal circuits appeared to occur in parallel. Efficient energy delivery by the entrained vasomotion may contribute to meeting the energy demand for increased coordinated neuronal activity and the subsequent neuronal circuit reorganization.
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- Medicine
- Neuroscience
Background:
Ketamine has emerged as one of the most promising therapies for treatment-resistant depression. However, inter-individual variability in response to ketamine is still not well understood and it is unclear how ketamine’s molecular mechanisms connect to its neural and behavioral effects.
Methods:
We conducted a single-blind placebo-controlled study, with participants blinded to their treatment condition. 40 healthy participants received acute ketamine (initial bolus 0.23 mg/kg, continuous infusion 0.58 mg/kg/hr). We quantified resting-state functional connectivity via data-driven global brain connectivity and related it to individual ketamine-induced symptom variation and cortical gene expression targets.
Results:
We found that: (i) both the neural and behavioral effects of acute ketamine are multi-dimensional, reflecting robust inter-individual variability; (ii) ketamine’s data-driven principal neural gradient effect matched somatostatin (SST) and parvalbumin (PVALB) cortical gene expression patterns in humans, while the mean effect did not; and (iii) behavioral data-driven individual symptom variation mapped onto distinct neural gradients of ketamine, which were resolvable at the single-subject level.
Conclusions:
These results highlight the importance of considering individual behavioral and neural variation in response to ketamine. They also have implications for the development of individually precise pharmacological biomarkers for treatment selection in psychiatry.
Funding:
This study was supported by NIH grants DP5OD012109-01 (A.A.), 1U01MH121766 (A.A.), R01MH112746 (J.D.M.), 5R01MH112189 (A.A.), 5R01MH108590 (A.A.), NIAAA grant 2P50AA012870-11 (A.A.); NSF NeuroNex grant 2015276 (J.D.M.); Brain and Behavior Research Foundation Young Investigator Award (A.A.); SFARI Pilot Award (J.D.M., A.A.); Heffter Research Institute (Grant No. 1–190420) (FXV, KHP); Swiss Neuromatrix Foundation (Grant No. 2016–0111) (FXV, KHP); Swiss National Science Foundation under the framework of Neuron Cofund (Grant No. 01EW1908) (KHP); Usona Institute (2015 – 2056) (FXV).
Clinical trial number:
