PubMed · 12230725
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Maurits van Tulder, Bart Koes. 2002. Low back pain and sciatica: chronic.. https://pubmed.ncbi.nlm.nih.gov/12230725/
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The present study was designed to characterize underlying mechanism involved in the development of tolerance in the production of antinociceptive effect induced by repeated cold water swimming stress (CWSS) using the tail-flick test. Mice were forced to swim at 4 degrees C for 3min and the tail-flick test was performed 5, 10, 20, and 30min after the swimming. The profound antinociception was induced by a single CWSS. However, when the mice were exposed to CWSS repeatedly seven times, they showed a tolerance in the production of antinociception. In the opioid receptor binding study, Bmax of delta opioid receptor (DOR) was decreased in the brainstem, midbrain and the spinal cord areas by both a single and repeated CWSS, without altering Kd value. However, Bmax values of mu opioid receptor (MOR) and kappa opioid receptor (KOR) were increased in the brainstem, midbrain and spinal cord regions by repeated CWSS, without changing Kd values. Our results suggest that the development of tolerance in the production of antinociception in mice forced to the repeated CWSS may be, at least, due to the reduction of DOR number in the brainstem, midbrain and the spinal cord regions.
Improgan, a chemical congener of the H(2) antagonist cimetidine, induces antinociception following intracerebroventricular (i.c.v.) administration in rodents, but the mechanism of action of this compound remains unknown. Because the chemical structure of improgan closely resembles those of histamine and certain histamine blockers, and because neuronal histamine is known to participate in pain-relieving responses, the antinociceptive actions of improgan were evaluated in mice containing null mutations in the genes for three histamine receptors (H(1), H(2), and H(3)) and also in the gene for histidine decarboxylase (the histamine biosynthetic enzyme). Similar to earlier findings in Swiss-Webster mice, improgan induced maximal, reversible, dose-related reductions in thermal nociceptive responses in ICR mice, but neither pre-improgan (baseline) nor post-improgan nociceptive latencies were changed in any of the mutant mice as compared with wild-type controls. Improgan also had weak inhibitory activity in vitro (pK(i)=4.7-4.9) on specific binding to three recently-discovered, recombinant isoforms of the rat H(3) receptor (H(3A), H(3B), and H(3C)). The present findings strongly support the hypothesis that neuronal histamine and its receptors fail to play a role in improgan-induced antinociception.
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