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}
}
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36 Citations
Highly Influential Citations
4
Background Citations
15
Methods Citations
4
Results Citations
1

36 Citations

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.
L-type Ca(2+) channel blockers inhibit the development but not the expression of sensitization to morphine in mice.
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.
Fluoxetine increases analgesic effects of morphine, prevents development of morphine tolerance and dependence through the modulation of L-type calcium channels expression in mice
The expression of a high level of morphine antinociceptive tolerance in mice involves both PKC and PKA
Role of kappa and delta opioid receptors in mediating morphine-induced antinociception in morphine-tolerant infant rats
PKC and PKA inhibitors reinstate morphine-induced behaviors in morphine tolerant mice.
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.
Involvement of hypothalamic pituitary adrenal axis on the analgesic cross-tolerance between morphine and nifedipine
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References

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Calcium modulation of morphine analgesia: role of calcium channels and intracellular pool calcium.
TLDR
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.
Effects of divalent cations, cation chelators and an ionophore on morphine analgesia and tolerance.
TLDR
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.
Opiate tolerance-induced modulation of free intracellular calcium in synaptosomes.
Calcium channel antagonists increase morphine-induced analgesia and antagonize morphine tolerance.
Prolonged morphine treatment increases rat brain dihydropyridine binding sites: possible involvement in development of morphine dependence.
MODIFICATION OF ENDORPHIN/ENKEPHALIN ANALGESIA AND STRESS‐INDUCED ANALGESIA BY DIVALENT CATIONS, A CATION CHELATOR AND AN IONOPHORE
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.
Differential effects of divalent cations, cation chelators and an ionophore (A23187) on morphine and dibutyryl guanosine 3': 5'-cyclic monophosphate antinociception.
TLDR
The results provide further evidence that the mechanism of db c-GMP antinociception is different from that of morphine.
Selective enhancement in striatal [3H]nitrendipine binding following chronic treatment with morphine
Calcium‐induced calcium release in rat sensory neurons.
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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