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Related Experiment Videos

Sensitivity changes after morphine treatment in the mouse uterus

E Contreras, L Tamayo, S Juica

    Archives Internationales De Pharmacodynamie Et De Therapie
    |January 1, 1982
    PubMed
    Summary

    Morphine pretreatment alters mouse uterine responses to acetylcholine and serotonin, inducing supersensitivity and tolerance. Methylxanthines like caffeine counteract these morphine-induced changes, suggesting a role in cellular calcium distribution.

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    Area of Science:

    • Pharmacology
    • Neuroscience
    • Reproductive Biology

    Background:

    • Morphine's effect on vas deferens suggests a dependence-like facilitatory action.
    • Previous research indicated morphine can induce dependence-like effects in smooth muscle preparations.

    Purpose of the Study:

    • To investigate if morphine pretreatment induces similar effects on mouse uterine contractile responses.
    • To examine the effects of acetylcholine and serotonin on uteri from morphine-pretreated mice.

    Main Methods:

    • Isolated mouse uteri were used to assess contractile responses.
    • Experiments involved acute morphine administration and long-term morphine pretreatment.
    • Responses to acetylcholine and serotonin were measured under various conditions, including naloxone and altered calcium concentrations.

    Main Results:

    • Acute morphine attenuated uterine responses to acetylcholine and serotonin in naive mice.
    • Long-term morphine pretreatment induced supersensitivity to these agonists and tolerance to morphine's depressant effect.
    • Methylxanthines (caffeine, theophylline) reduced tolerance in uteri from chronically morphinized mice.

    Conclusions:

    • Long-term morphine exposure induces a supersensitivity state and tolerance in the mouse uterus, distinct from its effects on the vas deferens.
    • Methylxanthines appear to oppose chronic morphine's effects, potentially by influencing intracellular calcium distribution.
    • Naloxone did not alter morphine's effects, suggesting opioid receptor-independent mechanisms in this context.

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