rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
21
|
pubmed:dateCreated |
2000-11-9
|
pubmed:abstractText |
The neuropeptide galanin is expressed developmentally in the dorsal root ganglion (DRG) and is rapidly up-regulated 120-fold after peripheral nerve section in the adult. Here we report that adult mice carrying a loss-of-function mutation in the galanin gene have a 13% reduction in the number of cells in the DRG associated with a 24% decrease in the percentage of neurons that express substance P. These deficits are associated with a 2.8- and 2.6-fold increase in the number of apoptotic cells in the DRG at postnatal days 3 and 4, respectively. After crush injury to the sciatic nerve, the rate of peripheral nerve regeneration is reduced by 35% with associated long-term functional deficits. Cultured DRG neurons from adult mutant mice demonstrate similar deficits in neurite number and length. These results identify a critical role for galanin in the development and regeneration of sensory neurons.
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pubmed:commentsCorrections |
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
10
|
pubmed:volume |
97
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
11563-8
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
|
pubmed:year |
2000
|
pubmed:articleTitle |
Targeted disruption of the galanin gene reduces the number of sensory neurons and their regenerative capacity.
|
pubmed:affiliation |
Departments of Medicine and Oral and Dental Science, Bristol University, Marlborough Street, Bristol BS2 8HW, United Kingdom.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|