Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-2-11
pubmed:abstractText
Because cholecystokinin (CCK) acts as a "functional" endogenous opioid antagonist, it has been proposed that changes in central CCKergic neurotransmission might account for the relative resistance of neuropathic pain to the analgesic action of morphine. This hypothesis was addressed by measuring CCK-related parameters 2 weeks after unilateral sciatic nerve section in rats. As expected, significant decreases (-25-38%) in the tissue concentrations and in vitro release of both substance P and calcitonin gene-related peptide were noted in the dorsal quadrant of the lumbar spinal cord on the lesioned side. In contrast, the tissue levels and in vitro release of CCK were unchanged in the same area in lesioned rats. Measurements in dorsal root ganglia at L4-L6 levels revealed no significant changes in proCCK mRNA after the lesion. However, sciatic nerve section was associated with a marked ipsilateral increase in both CCK-B receptor mRNA levels in these ganglia (+70%) and the autoradiographic labeling of CCK-B receptors by [3H]pBC 264 (+160%) in the superficial layers of the lumbar dorsal horn. Up-regulation of CCK-B receptors rather than CCK synthesis and release probably contributes to increased spinal CCKergic neurotransmission in neuropathic pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Calcitonin Gene-Related Peptide, http://linkedlifedata.com/resource/pubmed/chemical/Cholecystokinin, http://linkedlifedata.com/resource/pubmed/chemical/Potassium, http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Cholecystokinin B, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Calcitonin Gene-Related..., http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholecystokinin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-1, http://linkedlifedata.com/resource/pubmed/chemical/Substance P, http://linkedlifedata.com/resource/pubmed/chemical/Tachykinins, http://linkedlifedata.com/resource/pubmed/chemical/pro-calcitonin gene-related peptide, http://linkedlifedata.com/resource/pubmed/chemical/protachykinin
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
72
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
858-67
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9930763-Animals, pubmed-meshheading:9930763-Autoradiography, pubmed-meshheading:9930763-Axotomy, pubmed-meshheading:9930763-Calcitonin Gene-Related Peptide, pubmed-meshheading:9930763-Cholecystokinin, pubmed-meshheading:9930763-Ganglia, Spinal, pubmed-meshheading:9930763-Gene Expression, pubmed-meshheading:9930763-Male, pubmed-meshheading:9930763-Potassium, pubmed-meshheading:9930763-Protein Precursors, pubmed-meshheading:9930763-RNA, Messenger, pubmed-meshheading:9930763-Rats, pubmed-meshheading:9930763-Rats, Sprague-Dawley, pubmed-meshheading:9930763-Receptor, Cholecystokinin B, pubmed-meshheading:9930763-Receptors, Calcitonin Gene-Related Peptide, pubmed-meshheading:9930763-Receptors, Cholecystokinin, pubmed-meshheading:9930763-Receptors, Neurokinin-1, pubmed-meshheading:9930763-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:9930763-Sciatic Nerve, pubmed-meshheading:9930763-Spinal Cord, pubmed-meshheading:9930763-Substance P, pubmed-meshheading:9930763-Synaptic Transmission, pubmed-meshheading:9930763-Tachykinins
pubmed:year
1999
pubmed:articleTitle
Effects of peripheral axotomy on cholecystokinin neurotransmission in the rat spinal cord.
pubmed:affiliation
INSERM U 288, NeuroPsychoPharmacologie Moléculaire, Cellulaire et Fonctionnelle, Faculté de Médecine Pitié-Salpêtrière, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't