Linked Life Data

10199622

Source:http://linkedlifedata.com/resource/pubmed/id/10199622

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-7-7
pubmed:abstractText
A transgenic mouse has been developed which, during development, over-expresses nerve growth factor under the control of a myelin basic protein promoter. These animals display an ectopic network of substance P-containing sensory fibers in the white matter of the spinal cord. To study the functional significance of this model to nociception, these mice were studied in a test measuring the latency to tail withdrawal from a noxious radiant heat stimulus. Baseline reaction times were significantly less in transgenic mice, suggesting thermal allodynia. A mechanical stimulus was then applied to the tip of the tail at either 450 g or 1400 g for 2 s and tail withdrawal readings were taken for another 10 min. In control mice, the 450 g stimulus was without effect, suggesting that it is normally innocuous. In transgenic mice, this stimulus induced a transient decrease in withdrawal latency at 1 min. Thus, transgenic mice exhibited mechanical allodynia. The 1400 g stimulus decreased withdrawal latency in both transgenic and control mice. However, the response was greater in transgenic mice, indicating that they exhibited mechanical hyperalgesia. The neurokinin-1 receptor antagonist CP-96,345, but not the inactive stereoisomer CP-96,344, administered subcutaneously 30 min before the 450 g stimulus, blocked the stimulation-induced allodynia in transgenic mice, and revealed a transient antinociception in transgenic and control mice. Ketamine, an N-methyl-D-aspartate receptor antagonist, given intraperitoneally 10 min before 450 g stimulation, blocked the allodynia in transgenic mice. These results indicate that these transgenic mice display hyperalgesia and allodynia, and that these nociceptive responses are reversed by substance P and N-methyl-D-aspartate receptor antagonists.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
891-9
pubmed:dateRevised
2010-4-29
pubmed:meshHeading
pubmed-meshheading:10199622-Analgesics, pubmed-meshheading:10199622-Animals, pubmed-meshheading:10199622-Biphenyl Compounds, pubmed-meshheading:10199622-Excitatory Amino Acid Antagonists, pubmed-meshheading:10199622-Gene Expression Regulation, pubmed-meshheading:10199622-Hot Temperature, pubmed-meshheading:10199622-Hyperalgesia, pubmed-meshheading:10199622-Ketamine, pubmed-meshheading:10199622-Male, pubmed-meshheading:10199622-Mice, pubmed-meshheading:10199622-Mice, Transgenic, pubmed-meshheading:10199622-Myelin Basic Proteins, pubmed-meshheading:10199622-Nociceptors, pubmed-meshheading:10199622-Promoter Regions, Genetic, pubmed-meshheading:10199622-Reaction Time, pubmed-meshheading:10199622-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:10199622-Receptors, Neurokinin-1, pubmed-meshheading:10199622-Recombinant Fusion Proteins, pubmed-meshheading:10199622-Spinal Cord, pubmed-meshheading:10199622-Stress, Mechanical, pubmed-meshheading:10199622-Substance P
pubmed:year
1999
pubmed:articleTitle
Transgenic mice over-expressing substance P exhibit allodynia and hyperalgesia which are reversed by substance P and N-methyl-D-aspartate receptor antagonists.
pubmed:affiliation
Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't