Involvement of Intracellular Calcium in Morphine Tolerance in Mice

@article{Smith1999InvolvementOI,
  title={Involvement of Intracellular Calcium in Morphine Tolerance in Mice},
  author={Forrest L. Smith and Daniel S. Dombrowski and William L. Dewey},
  journal={Pharmacology Biochemistry and Behavior},
  year={1999},
  volume={62},
  pages={381-388}
}
Involvement of phospholipid signal transduction pathways in morphine tolerance in mice
TLDR
Evidence is accumulating that opioid tolerance disrupts the homeostatic balance of several important signal transduction pathways and a potential role for inositol 1,4,5‐trisphosphate (IP3) and protein kinase C (PKC) in tolerance is suggested.
Blocking the R‐type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance
TLDR
The inhibition of R‐type Ca2+ current could lead to high‐efficiency opioid therapy without tolerance, as it is speculated that voltage‐dependent Ca3+ channels play a key role in morphine analgesia and tolerance.
Role of CD38, a Cyclic ADP-Ribosylcyclase, in Morphine Antinociception and Tolerance
TLDR
Results indicate that cADRP–ryanodine receptor Ca2+ signaling associated with CD38 plays an important role in morphine tolerance.
COMPARISON OF ACUTE AND CHRONIC EFFECTS OF NIFEDIPINE ON NALOXONE-PRECIPITATED MORPHINE WITHDRAWAL IN MICE
TLDR
The results suggest that alterations in dihydropyridine-sensitive calcium channels may be involved in the adaptations that occur on chronic treatment with morphine, and that separate mechanisms areinvolved in the development of tolerance and dependence.
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Results of this study indicate that Ca++ blocked morphine antinociception by stimulating Ca++ influx through omega-conotoxin GVIA-sensitive channels and by stimulated Ca++ release from Ca++/caffeine-sensitive microsomal pools.
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It is found that Ca"++ must penetrate cell membranes in order to reduce the analgesic effects of morphine, indicating the importance of Ca++ localization in the actions of narcotic agonists and antagonists.
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TLDR
Previous findings indicating that divalent metal ions (and especially Ca2+) may be involved in the actions of opiates were confirmed, suggesting antagonism of endogenous opiates.
Calcium channel inhibitors suppress the morphine‐withdrawal syndrome in rats
TLDR
The results suggest that Ca2+‐channel blockers suppress the behavioural and neurochemical expressions of morphine abstinence by a mechanism that differs from those of opioids or α2‐adrenoceptor agonists.
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TLDR
The results provide further evidence that the mechanism of db c-GMP antinociception is different from that of morphine.
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TLDR
The results suggest that Ca(2+)‐induced Ca2+ release (CICR) is expressed differently in different populations of DRG neurons, and it is discussed that CICR can contribute to the depolarization‐induced [Ca2+]c, provided the Ca2- influx lasts for a certain minimum period of time.
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