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Related Experiment Videos

On the mechanism of the decrease in cerebellar cyclic GMP content elicited by opiate receptor agonists.

G Biggio, A Guidotti, E Costa

    Naunyn-Schmiedeberg'S Archives of Pharmacology
    |January 1, 1977
    PubMed
    Summary

    Morphine and related drugs reduce cyclic guanosine monophosphate (cGMP) in the rat cerebellum. This effect, mediated by striatal opiate receptors, suggests a link between opioid signaling and cerebellar function.

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    Area of Science:

    • Neuroscience
    • Pharmacology
    • Biochemistry

    Background:

    • Cyclic guanosine monophosphate (cGMP) plays a role in neuronal signaling.
    • Opioid receptors are known to modulate various brain functions.

    Purpose of the Study:

    • To investigate the effect of morphine and related analgesics on cerebellar cGMP levels.
    • To determine the brain regions and receptor systems involved in morphine's action on cerebellar cGMP.

    Main Methods:

    • Administration of morphine, dextromoramide, and vimonol R2 to rats.
    • Measurement of cGMP content in rat cerebellar cortex and deep cerebellar nuclei.
    • Intrastriatal and intracerebellar injections of morphine.
    • Administration of naltrexone and apomorphine to assess receptor involvement.

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  • Pretreatment with 3-acetylpyridine to investigate the role of climbing fibers.
  • Main Results:

    • Analgesic doses of morphine, dextromoramide, and vimonol R2 decreased cerebellar cGMP.
    • Intrastriatal morphine, but not intracerebellar, reduced cerebellar cGMP.
    • The effect of morphine was blocked by apomorphine (dopaminergic agonist) but not naltrexone (opiate antagonist).
    • 3-acetylpyridine pretreatment did not prevent the reduction of cerebellar cGMP by morphine.

    Conclusions:

    • Activation of striatal opiate receptors by morphine leads to a decrease in cerebellar cGMP.
    • This reduction in cGMP is likely mediated by a decrease in excitatory mossy fiber input to the cerebellum.
    • The findings suggest a novel pathway linking striatal opioid activity to cerebellar function.