Unusual prism adaptation reveals how grasping is controlled

  1. Willemijn D Schot  Is a corresponding author
  2. Eli Brenner  Is a corresponding author
  3. Jeroen BJ Smeets  Is a corresponding author
  1. Vrije Universiteit Amsterdam, Netherlands

Abstract

There are three main theories on how human grasping movements are controlled. Two of them state that grip aperture and the movement of the hand are controlled. They differ in whether the wrist or the thumb of the hand is controlled. We have proposed a third theory, which states that grasping is a combination of two goal-directed single-digit movements, each directed at a specific position on the object. In this study, we test predictions based on each of the theories by examining the transfer of prism adaptation during single-digit pointing movements to grasping movements. We show that adaptation acquired during single-digit movements transfers to the hand opening when subsequently grasping objects, leaving the movement of the hand unaffected. Our results provide strong evidence for our theory that grasping with the thumb and index finger is based on a combination of two goal-directed single-digit movements.

Article and author information

Author details

  1. Willemijn D Schot

    Department of Human Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, Netherlands
    For correspondence
    W.D.Schot@uu.nl
    Competing interests
    The authors declare that no competing interests exist.
  2. Eli Brenner

    Department of Human Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, Netherlands
    For correspondence
    E.Brenner@vu.nl
    Competing interests
    The authors declare that no competing interests exist.
  3. Jeroen BJ Smeets

    Department of Human Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, Netherlands
    For correspondence
    J.B.J.Smeets@vu.nl
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-3794-0579

Funding

Nederlandse Organisatie voor Wetenschappelijk Onderzoek (453-08-004)

  • Jeroen BJ Smeets

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

Ethics

Human subjects: This study was part of a research programme that has been approved by the Ethische Commissie Bewegingswetenschappen (ECB 2006-02). All participants gave their informed consent before participating in this study.

Reviewing Editor

  1. Richard Ivry, University of California, Berkeley, United States

Publication history

  1. Received: September 11, 2016
  2. Accepted: September 9, 2017
  3. Accepted Manuscript published: September 11, 2017 (version 1)
  4. Version of Record published: September 28, 2017 (version 2)

Copyright

© 2017, Schot 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.

Metrics

  • 942
    Page views
  • 140
    Downloads
  • 5
    Citations

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)

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. Willemijn D Schot
  2. Eli Brenner
  3. Jeroen BJ Smeets
(2017)
Unusual prism adaptation reveals how grasping is controlled
eLife 6:e21440.
https://doi.org/10.7554/eLife.21440

Further reading

    1. Neuroscience
    Kelly M Martyniuk et al.
    Research Article Updated

    In the striatum, acetylcholine (ACh) neuron activity is modulated co-incident with dopamine (DA) release in response to unpredicted rewards and reward-predicting cues and both neuromodulators are thought to regulate each other. While this co-regulation has been studied using stimulation studies, the existence of this mutual regulation in vivo during natural behavior is still largely unexplored. One long-standing controversy has been whether striatal DA is responsible for the induction of the cholinergic pause or whether DA D2 receptors (D2Rs) modulate a pause that is induced by other mechanisms. Here, we used genetically encoded sensors in combination with pharmacological and genetic inactivation of D2Rs from cholinergic interneurons (CINs) to simultaneously measure ACh and DA levels after CIN D2R inactivation in mice. We found that CIN D2Rs are not necessary for the initiation of cue-induced decrease in ACh levels. Rather, they prolong the duration of the decrease and inhibit ACh rebound levels. Notably, the change in cue-evoked ACh levels is not associated with altered cue-evoked DA release. Moreover, D2R inactivation strongly decreased the temporal correlation between DA and ACh signals not only at cue presentation but also during the intertrial interval pointing to a general mechanism by which D2Rs coordinate both signals. At the behavioral level D2R antagonism increased the latency to lever press, which was not observed in CIN-selective D2R knock out mice. Press latency correlated with the cue-evoked decrease in ACh levels and artificial inhibition of CINs revealed that longer inhibition shortens the latency to press compared to shorter inhibition. This supports a role of the ACh signal and it’s regulation by D2Rs in the motivation to initiate actions.

    1. Cell Biology
    2. Neuroscience
    Lauritz Kennedy et al.
    Research Article

    Neonatal cerebral hypoxia-ischemia (HI) is the leading cause of death and disability in newborns with the only current treatment being hypothermia. An increased understanding of the pathways that facilitate tissue repair after HI may aid the development of better treatments. Here, we study the role of lactate receptor HCAR1 in tissue repair after neonatal HI in mice. We show that HCAR1 knockout mice have reduced tissue regeneration compared with wildtype mice. Furthermore, proliferation of neural progenitor cells and glial cells, as well as microglial activation was impaired. Transcriptome analysis showed a strong transcriptional response to HI in the subventricular zone of wildtype mice involving about 7300 genes. In contrast, the HCAR1 knockout mice showed a modest response, involving about 750 genes. Notably, fundamental processes in tissue repair such as cell cycle and innate immunity were dysregulated in HCAR1 knockout. Our data suggest that HCAR1 is a key transcriptional regulator of pathways that promote tissue regeneration after HI.