Document Detail


Temporal evolution of "automatic gain-scaling".
MedLine Citation:
PMID:  19439680     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The earliest neural response to a mechanical perturbation, the short-latency stretch response (R1: 20-45 ms), is known to exhibit "automatic gain-scaling" whereby its magnitude is proportional to preperturbation muscle activity. Because gain-scaling likely reflects an intrinsic property of the motoneuron pool (via the size-recruitment principle), counteracting this property poses a fundamental challenge for the nervous system, which must ultimately counter the absolute change in load regardless of the initial muscle activity (i.e., show no gain-scaling). Here we explore the temporal evolution of gain-scaling in a simple behavioral task where subjects stabilize their arm against different background loads and randomly occurring torque perturbations. We quantified gain-scaling in four elbow muscles (brachioradialis, biceps long, triceps lateral, triceps long) over the entire sequence of muscle activity following perturbation onset-the short-latency response, long-latency response (R2: 50-75 ms; R3: 75-105 ms), early voluntary corrections (120-180 ms), and steady-state activity (750-1250 ms). In agreement with previous observations, we found that the short-latency response demonstrated substantial gain-scaling with a threefold increase in background load resulting in an approximately twofold increase in muscle activity for the same perturbation. Following the short-latency response, we found a rapid decrease in gain-scaling starting in the long-latency epoch ( approximately 75-ms postperturbation) such that no significant gain-scaling was observed for the early voluntary corrections or steady-state activity. The rapid decrease in gain-scaling supports our recent suggestion that long-latency responses and voluntary control are inherently linked as part of an evolving sensorimotor control process through similar neural circuitry.
Authors:
J Andrew Pruszynski; Isaac Kurtzer; Timothy P Lillicrap; Stephen H Scott
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-13
Journal Detail:
Title:  Journal of neurophysiology     Volume:  102     ISSN:  0022-3077     ISO Abbreviation:  J. Neurophysiol.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-08-03     Completed Date:  2009-09-24     Revised Date:  2010-09-27    
Medline Journal Info:
Nlm Unique ID:  0375404     Medline TA:  J Neurophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  992-1003     Citation Subset:  IM    
Affiliation:
Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6, Canada.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Biomechanics
Elasticity
Elbow / physiology*
Electromyography
Hand
Humans
Models, Biological*
Motor Activity / physiology*
Muscle, Skeletal / physiology*
Regression Analysis
Time Factors
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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