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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-11-26
pubmed:abstractText
The increase in pain sensitivity that follows injury is regulated by superficially located projection neurons in the dorsal horn of the spinal cord that express the neurokinin-1 (NK1) receptor. After selective ablation of these neurons in rats, we identified changes in receptive field size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that are important for both pain sensations and reflexes. We were able to reproduce these changes by pharmacological block of descending serotonergic facilitatory pathways. Using Fos histochemistry, we found changes in the activation of serotonergic neurons in the brainstem as well as evidence for a loss of descending control of spinal excitability. We conclude that NK1-positive spinal projection neurons, activated by primary afferent input, project to higher brain areas that control spinal excitability--and therefore pain sensitivity--primarily through descending pathways from the brainstem.
pubmed:language
eng
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:author
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1319-26
pubmed:dateRevised
2007-11-15
pubmed:articleTitle
Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways.
pubmed:affiliation
Department of Pharmacology, University College London, Gower Street, London WC1E 6BT, UK. ucklrsu@ucl.ac.uk