Document Detail


Overexpression of neurotrophin-3 in skeletal muscle alters normal and injury-induced limb control.
MedLine Citation:
PMID:  11794730     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transgenic overexpression of neurotrophin-3 (NT-3) in mice increases the number of surviving proprioceptive sensory components, including primary sensory neurons, gamma motoneurons and muscle spindles. The numbers of surviving alpha motoneurons are not affected by NT-3 overexpression (Wright et al., Neuron 19: 503-517, 1997). We have assessed the consequences NT-3-stimulated increase in the proprioceptive sensory system by measuring locomotive abilities of mice that overexpress NT-3 in all skeletal muscles (myo/NT-3 mice). In adulthood, one myo/NT-3 transgenic line continues to express NT-3 at high levels in muscle and maintains a hypertrophied proprioceptive system (high-OE myo/NT-3 mice). Compared to wildtypes, high-OE myo/NT-3 mice have nine times the amount of NT-3 protein in the medial gastrocnemius at six weeks of age. Although appearing normal during ordinary activity, high-OE myo/NT-3 mice display a distinct clasping phenotype when lifted by the tail. High-OE myo/NT-3 mice show severe locomotor deficits when performing beam walking and rotorod testing. These mice also demonstrate aberrant foot positioning during normal walking. However, following sciatic nerve crush, overexpression of NT-3 prevents further abnormalities in paw positioning, suggesting NT-3 may attenuate sensorimotor deficits that occur in response to sciatic nerve injury. Our results suggest that increases in proprioceptive sensory neurons, spindles and gamma motoneurons, along with continued postnatal NT-3 overexpression in muscle significantly disrupt normal locomotor control. Importantly, however, NT-3 may lessen initial deficits and thus improve functional recovery after peripheral nerve injury, suggesting these mice may serve as a good model to study NT-3's role in neuroprotection of proprioceptive afferents.
Authors:
M D Taylor; R Vancura; J M Williams; J T Riekhof; B K Taylor; D E Wright
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Somatosensory & motor research     Volume:  18     ISSN:  0899-0220     ISO Abbreviation:  Somatosens Mot Res     Publication Date:  2001  
Date Detail:
Created Date:  2002-01-16     Completed Date:  2002-06-14     Revised Date:  2013-07-15    
Medline Journal Info:
Nlm Unique ID:  8904127     Medline TA:  Somatosens Mot Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  286-94     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City 66160, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Extremities / innervation*,  physiology*
Gait
Gene Expression Regulation / physiology*
Hindlimb / physiology
Mice
Mice, Transgenic
Muscle, Skeletal / metabolism*
Myogenin / genetics
Nerve Crush
Neurons, Afferent / physiology
Neuroprotective Agents
Neurotrophin 3 / biosynthesis*,  genetics
Postural Balance / physiology
Promoter Regions, Genetic / physiology
Proprioception / physiology
Psychomotor Performance / physiology
Sciatic Nerve / injuries*
Grant Support
ID/Acronym/Agency:
DE07734/DE/NIDCR NIH HHS; NS37910/NS/NINDS NIH HHS; R01 NS043314/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Myog protein, mouse; 0/Myogenin; 0/Neuroprotective Agents; 0/Neurotrophin 3

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


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