Linked Life Data

18498707

Source:http://linkedlifedata.com/resource/pubmed/id/18498707

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-5-23
pubmed:abstractText
Mechanical allodynia, such as static and dynamic allodynia, is a prominent feature of neuropathic pain syndromes. The aim of this study is to characterize primary sensory neurons mediating the mechanical allodynia in a rat chronic constriction injury (CCI) model with a combination of pharmacological and histological investigations. N-(4-Tertiarybutylphenyl)-4-(3-chloropyridin-2-yl) tetrahydropyrazine-1(2H)-carbox-amide (BCTC), a selective and competitive antagonist of the vanilloid receptor 1 (TRPV1), and resiniferatoxin, which causes desensitization of TRPV1-expressing fibres, suppressed static allodynia but not dynamic allodynia in CCI rats. Immunohistochemical studies of TRPV1 and NF200, an A-fibre marker 200 kDa neurofilament, in dorsal root ganglion neurons demonstrated that each 48% of the positive-stained neurons were immunoreactive only for TRPV1 or NF200. The other 4% of stained neurons were double-positive for TRPV1 and NF200. Of the TRPV1positive neurons, more than 99% were small-(diameter <25 microm) and medium-(25-45 microm) sized. In contrast, 97% of NF200 single-labelled neurons were medium-and large-(>45 microm) sized. These findings suggest that two types of mechanical allodynia are transmitted by different primary sensory neurons: static allodynia is mediated by TRPV1 positive small-and medium-sized neurons and dynamic allodynia might be signalled by TRPV1-negative medium- and large-sized neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-3573
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
717-22
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Characterization of primary sensory neurons mediating static and dynamic allodynia in rat chronic constriction injury model.
pubmed:affiliation
Discovery Biology Research, Nagoya Laboratories, Pfizer Global Research and Development, Pfizer Inc., 5-2, Taketoyo, Aichi, 470-2393, Japan.
pubmed:publicationType
Journal Article