Linked Life Data

16488412

Source:http://linkedlifedata.com/resource/pubmed/id/16488412

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-4-17
pubmed:abstractText
Under normal conditions, expression of the p75 neurotrophin receptor (p75NTR) by sympathetic neurons can increase the affinity of the signaling receptor, trkA, to target-derived nerve growth factor (NGF) at distal axons. We have previously reported that sprouting of sympathetic axons into NGF-rich target tissues is enhanced when p75NTR expression is perturbed, leading to the postulate that p75NTR may restrain sympathetic sprouting in response to elevated NGF levels. These observations were made using mice having a null mutation of the third p75NTR exon, a line that may express a hypomorphic form of this receptor. Since mice carrying a null mutation of the fourth p75NTR exon may not express a similar splice variant, we sought to determine whether these animals possess the same phenotype of enhanced sympathetic sprouting in response to elevated levels of NGF. Both lines of transgenic mice lacking p75NTR displayed similar degrees of sympathetic axonal sprouting into the cerebellum and trigeminal ganglia, two target tissues having elevated levels of NGF protein. Furthermore, the densities of sympathetic axons in both targets were significantly greater than those observed in age-matched NGF transgenic siblings expressing full-length p75NTR. Our new findings provide a comparative analysis of the phenotype in two independent mutations of the same neurotrophin receptor, revealing that p75NTR plays an important role in restricting sympathetic sprouting in response to higher NGF levels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
198
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
416-26
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16488412-Animals, pubmed-meshheading:16488412-Cell Count, pubmed-meshheading:16488412-Cell Enlargement, pubmed-meshheading:16488412-Cerebellum, pubmed-meshheading:16488412-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:16488412-Exons, pubmed-meshheading:16488412-Immunohistochemistry, pubmed-meshheading:16488412-Mice, pubmed-meshheading:16488412-Mice, Knockout, pubmed-meshheading:16488412-Mutation, pubmed-meshheading:16488412-Nerve Growth Factor, pubmed-meshheading:16488412-Neurites, pubmed-meshheading:16488412-Neurons, pubmed-meshheading:16488412-Neuropeptide Y, pubmed-meshheading:16488412-Receptor, Nerve Growth Factor, pubmed-meshheading:16488412-Receptor, trkA, pubmed-meshheading:16488412-Superior Cervical Ganglion, pubmed-meshheading:16488412-Sympathetic Nervous System, pubmed-meshheading:16488412-Trigeminal Ganglion, pubmed-meshheading:16488412-Tyrosine 3-Monooxygenase
pubmed:year
2006
pubmed:articleTitle
Null mutations for exon III and exon IV of the p75 neurotrophin receptor gene enhance sympathetic sprouting in response to elevated levels of nerve growth factor in transgenic mice.
pubmed:affiliation
Department of Anatomy and Cell Biology, Queen's University, Kingston, ON, Canada K7L 3N6.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural