ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract : Because cholecystokinin (CCK) acts as a“functional” endogenous opioid antagonist, it has been proposedthat changes in central CCKergic neurotransmission might account for therelative resistance of neuropathic pain to the analgesic action of morphine.This hypothesis was addressed by measuring CCK-related parameters 2 weeksafter unilateral sciatic nerve section in rats. As expected, significantdecreases (-25-38%) in the tissue concentrations and in vitro release of bothsubstance P and calcitonin gene-related peptide were noted in the dorsalquadrant of the lumbar spinal cord on the lesioned side. In contrast, thetissue levels and in vitro release of CCK were unchanged in the same area inlesioned rats. Measurements in dorsal root ganglia at L4-L6 levels revealed nosignificant changes in proCCK mRNA after the lesion. However, sciatic nervesection was associated with a marked ipsilateral increase in both CCK-Breceptor mRNA levels in these ganglia (+70%) and the autoradiographic labelingof 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1471-4159.1999.720858.x
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