Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-5-27
pubmed:abstractText
To assess the role of alpha(1G) T-type Ca2+ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking CaV3.1 (alpha1G(-/-)), the gene encoding the pore-forming units of these channels. Reduced spontaneous pain responses and an increased threshold for paw withdrawal in response to mechanical stimulation were observed in these mice. The alpha1G(-/-) mice also showed attenuated thermal hyperalgesia in response to both low-(IR30) and high-intensity (IR60) infrared stimulation. Our results reveal the importance of alpha(1G) T-type Ca2+ channels in the development of neuropathic pain, and suggest that selective modulation of alpha1G subtype channels may provide a novel approach to the treatment of allodynia and hyperalgesia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1016-8478
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
242-6
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Attenuated neuropathic pain in Cav3.1 null mice.
pubmed:affiliation
Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't