Linked Life Data

11234752

Source:http://linkedlifedata.com/resource/pubmed/id/11234752

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-3-7
pubmed:abstractText
Sensory neurones co-express voltage-gated sodium channels that mediate TTX-sensitive (TTX-S) and TTX-resistant (TTX-R) currents, which may contribute to chronic pain after nerve injury. We previously demonstrated that TTX-R channels were decreased acutely in human sensory cell bodies after central axotomy, but accumulated in nerve terminals after peripheral axotomy. We have now studied the TTX-S channels PN1 and Brain III, using specific antibodies for immunohistochemistry, in dorsal root ganglia (DRG) from 10 patients with traumatic central axotomy, nerves from 16 patients with peripheral axotomy, and controls. PN1 showed temporal changes similar to the TTX-R channels in sensory cell bodies of injured DRG. In contrast, Brain III was found only in injured nerves (not control nerves, or control/central axotomy DRG). PNI and Brain III are distinct targets for novel analgesics.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
495-500
pubmed:dateRevised
2005-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Plasticity of TTX-sensitive sodium channels PN1 and brain III in injured human nerves.
pubmed:affiliation
Department of Neurology, Imperial College of Science, Technology and Medicine, Hammersmith Hospital, London, UK.
pubmed:publicationType
Journal Article