Source:http://linkedlifedata.com/resource/pubmed/id/16452675
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2006-2-2
|
| pubmed:abstractText |
Adult facial motor neurons continue to express full-length TrkB tyrosine kinase receptor (TrkB.FL), the high-affinity receptor for the neurotrophins BDNF and neurotrophic factor-4/5 (NT-4/5), suggesting that they remain dependent on target-derived and locally produced neurotrophins in adulthood. Studies on the role of TrkB signaling in the adult CNS have been hampered by the early lethality of bdnf, nt-4/5, and trkB knock-out mice. We disrupted TrkB.FL signaling in adult facial motor neurons using adeno-associated viral vector-mediated overexpression of a naturally occurring dominant-negative TrkB receptor, TrkB.T1. Expression of TrkB.T1 resulted in neuronal atrophy and downregulation of NeuN (neuronal-specific nuclear protein) and ChAT expression in facial motor neurons. A subset of transduced neurons displayed signs of motor neuron degeneration that included dendritic beading and rounding of the soma at 2 months of TrkB.T1 expression. Cell counts revealed a significant reduction in motor neuron number in the facial nucleus at 4 months after onset of expression of TrkB.T1, suggesting that a proportion of TrkB.T1-expressing motor neurons became undetectable as a result of severe atrophy or was lost because of cell death. In contrast, overexpression of TrkB.FL did not result in a decrease in facial motor neuron number. Our results indicate that a subset of facial motor neurons remains dependent on TrkB ligands for the maintenance of structural and molecular characteristics in adulthood.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1529-2401
|
| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:day |
1
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1516-30
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:16452675-Animals,
pubmed-meshheading:16452675-Atrophy,
pubmed-meshheading:16452675-Cell Line,
pubmed-meshheading:16452675-Dendrites,
pubmed-meshheading:16452675-Dependovirus,
pubmed-meshheading:16452675-Down-Regulation,
pubmed-meshheading:16452675-Facial Nerve,
pubmed-meshheading:16452675-Gene Expression,
pubmed-meshheading:16452675-Genetic Vectors,
pubmed-meshheading:16452675-Humans,
pubmed-meshheading:16452675-Male,
pubmed-meshheading:16452675-Motor Neurons,
pubmed-meshheading:16452675-Nerve Degeneration,
pubmed-meshheading:16452675-Nerve Tissue Proteins,
pubmed-meshheading:16452675-Protein Isoforms,
pubmed-meshheading:16452675-Rats,
pubmed-meshheading:16452675-Rats, Wistar,
pubmed-meshheading:16452675-Receptor, trkB,
pubmed-meshheading:16452675-Recombinant Fusion Proteins,
pubmed-meshheading:16452675-Sequence Deletion,
pubmed-meshheading:16452675-Time Factors
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Long-term adeno-associated viral vector-mediated expression of truncated TrkB in the adult rat facial nucleus results in motor neuron degeneration.
|
| pubmed:affiliation |
Graduate School of Neuroscience, Netherlands Institute for Brain Research, 1105 AZ Amsterdam, The Netherlands.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|