Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-6-27
pubmed:abstractText
Motoneuron death leads to muscle denervation and atrophy. Transplantation of embryonic neurons into peripheral nerves results in reinnervation and provides a strategy to rescue muscles from atrophy independent of neuron replacement in a damaged or diseased spinal cord. But the count of regenerating axons always exceeds the number of motor units in this model, so target-derived trophic factor levels may limit reinnervation. Our aim was to examine whether long-term infusion of fibroblast growth factor-6 (FGF-6) into denervated medial gastrocnemius muscles improved the function of muscles reinnervated from neurons transplanted into nerve of adult Fischer rats. Factor delivery (10 microg, 4 weeks) began after sciatic nerve transection. After a week of nerve degeneration, 1 million embryonic day 14-15 ventral spinal cord cells were transplanted into the distal tibial stump as a neuron source. Ten weeks later, neurons that expressed motoneuron markers survived in the nerves. More myelinated axons were in nerves to saline-treated muscles than in FGF-6-treated muscles. However, each group showed comparable reductions in muscle fiber atrophy because of reinnervation. Mean reinnervated fiber area was 43%-51% of non-denervated fibers. Denervated fiber area averaged 11%. FGF-6-treated muscles were more fatigable than other reinnervated muscles but had stronger motor units and fewer type I fibers than did saline-treated muscles. FGF-6 thus influenced function by changing the type of fiber reinnervated by transplanted neurons. Deficits in FGF-6 may also contribute to the increase in type I fibers in muscles reinnervated from peripheral axons, suggesting that the effects of FGF-6 on fiber type are independent of the neuron source used for reinnervation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0360-4012
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1933-42
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17492788-Animals, pubmed-meshheading:17492788-Atrophy, pubmed-meshheading:17492788-Axons, pubmed-meshheading:17492788-Cell Count, pubmed-meshheading:17492788-Cell Survival, pubmed-meshheading:17492788-Cell Transplantation, pubmed-meshheading:17492788-Female, pubmed-meshheading:17492788-Fibroblast Growth Factor 6, pubmed-meshheading:17492788-Immunohistochemistry, pubmed-meshheading:17492788-Motor Neurons, pubmed-meshheading:17492788-Muscle, Skeletal, pubmed-meshheading:17492788-Muscle Fatigue, pubmed-meshheading:17492788-Muscle Fibers, Skeletal, pubmed-meshheading:17492788-Muscle Fibers, Slow-Twitch, pubmed-meshheading:17492788-Nerve Fibers, Myelinated, pubmed-meshheading:17492788-Nerve Regeneration, pubmed-meshheading:17492788-Neuromuscular Junction, pubmed-meshheading:17492788-Neurons, pubmed-meshheading:17492788-Peripheral Nerves, pubmed-meshheading:17492788-Proto-Oncogene Proteins, pubmed-meshheading:17492788-Rats, pubmed-meshheading:17492788-Rats, Inbred F344
pubmed:year
2007
pubmed:articleTitle
Long-term delivery of FGF-6 changes the fiber type and fatigability of muscle reinnervated from embryonic neurons transplanted into adult rat peripheral nerve.
pubmed:affiliation
The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida 33136-2104, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural