September 2017
Volume 17, Issue 10
Open Access
Vision Sciences Society Annual Meeting Abstract  |   August 2017
Neural markers of efficient response inhibition in parietal cortex
Author Affiliations
  • Tamar Kolodny
    Department of Cognitive Sciences, the Hebrew University of Jerusalem.
  • Pnina Stern
    Constantiner School of Education, Tel Aviv University.
  • Maya Ankaoua
    Sagol School of Neuroscience, Tel Aviv University.
  • Natalie Kataev
    School of Psychology, Tel Aviv University.
  • Shlomit Tsafrir
    Clalit Health Services, Israel.
  • Carmel Mevorach
    School of Psychology, University of Birmingham, UK.
  • Lilach Shalev
    Constantiner School of Education, Tel Aviv University.
    Sagol School of Neuroscience, Tel Aviv University.
Journal of Vision August 2017, Vol.17, 519. doi:10.1167/17.10.519
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      Tamar Kolodny, Pnina Stern, Maya Ankaoua, Natalie Kataev, Shlomit Tsafrir, Carmel Mevorach, Lilach Shalev; Neural markers of efficient response inhibition in parietal cortex. Journal of Vision 2017;17(10):519. doi: 10.1167/17.10.519.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Introduction: Response inhibition, the ability to suppress inadequate but prepotent response tendencies, is a cognitive-motor effortful process. Brain mechanisms typically reported for response inhibition are extensive, and there is an ongoing controversy evolving mainly around the role of frontal regions. In the current study we assessed response inhibition using a novel Go/No-go design and fMRI. Furthermore, we examined participants with attention-deficits/hyperactivity disorder (ADHD), a population with prominent dysfunction of response inhibition, to investigate brain correlates of atypical inhibition. Method: Using fMRI we recorded brain activity while participants performed a Go/No-go task with frequency manipulation of trial type. Although inhibition is required in all No-go trials, rare-No-go cases (25%) create a prepotent response and a strong demand for inhibition, while prevalent-No-go cases (75%) require very little inhibition effort. Thus, contrasting No-go trials from these different contexts pinpoints inhibition-related brain activation. Furthermore, among participants with ADHD, we assessed behavioral symptom severity using the Adult ADHD Self-Report Scale (ASRS), and examined the relationship between ADHD symptoms and inhibition-related brain activation. Results: Unlike previous reports, our unique design allowed us to isolate distinct clusters of activation in bilateral intraparietal sulcus (IPS) and left temporoparietal junction (TPJ). These regions showed greater activation to rare-No-go trials than to prevalent-No-go trials in healthy controls. Interestingly, this effect was absent in the ADHD group. Strikingly, parietal modulation by inhibition demand was associated with ADHD symptom severity, such that higher severity corresponded to reduced modulation in parietal cortex. Conclusions: Results of the current study highlight the contribution of the parietal cortex to inhibitory processes, while casting doubts on the specificity of frontal activation in such processes. Furthermore, we argue that elevated activity in bilateral IPS and left TPJ may serve as a neural marker of efficient inhibition of a pre-potent response and may be useful in identifying atypicalities.

Meeting abstract presented at VSS 2017

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