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J Neurophysiol. 2014 Jun 15;111(12):2544-53. doi: 10.1152/jn.00673.2013. Epub 2014 Mar 26.

Long-latency, inhibitory spinal pathway to ankle flexors activated by homonymous group 1 afferents.

Author information

  • 1Department of Biomedical Engineering, University of Alberta, Edmonton, Canada; Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada.
  • 2Department of Surgery, University of Alberta, Edmonton, Canada; Centre for Neuroscience, University of Alberta, Edmonton, Canada; Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada.
  • 3Centre for Neuroscience, University of Alberta, Edmonton, Canada;
  • 4Department of Physical Therapy, University of Alberta, Edmonton, Canada; Centre for Neuroscience, University of Alberta, Edmonton, Canada; Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada; and.
  • 5Department of Biomedical Engineering, University of Alberta, Edmonton, Canada; Centre for Neuroscience, University of Alberta, Edmonton, Canada; Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada monica.gorassini@ualberta.ca.

Abstract

Inhibitory feedback from sensory pathways is important for controlling movement. Here, we characterize, for the first time, a long-latency, inhibitory spinal pathway to ankle flexors that is activated by low-threshold homonymous afferents. To examine this inhibitory pathway in uninjured, healthy participants, we suppressed motor-evoked potentials (MEPs), produced in the tibialis anterior (TA), by a prior stimulation to the homonymous common peroneal nerve (CPN). The TA MEP was suppressed by a triple-pulse stimulation to the CPN, applied 40, 50, and 60 ms earlier and at intensities of 0.5-0.7 times motor threshold (average suppression of test MEP was 33%). Whereas the triple-pulse stimulation was below M-wave and H-reflex threshold, it produced a long-latency inhibition of background muscle activity, approximately 65-115 ms after the CPN stimulation, a time period that overlapped with the test MEP. However, not all of the MEP suppression could be accounted for by this decrease in background muscle activity. Evoked responses from direct activation of the corticospinal tract, at the level of the brain stem or thoracic spinal cord, were also suppressed by low-threshold CPN stimulation. Our findings suggest that low-threshold muscle and cutaneous afferents from the CPN activate a long-latency, homonymous spinal inhibitory pathway to TA motoneurons. We propose that inhibitory feedback from spinal networks, activated by low-threshold homonymous afferents, helps regulate the activation of flexor motoneurons by the corticospinal tract.

Copyright © 2014 the American Physiological Society.

KEYWORDS:

common peroneal nerve; spinal inhibition; tibialis anterior

PMID:
24671544
[PubMed - in process]
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