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Related Experiment Videos

Opiates, cyclic nucleotides, and xanthines.

H O Collier, D L Francis, A C Roy

    Advances in Biochemical Psychopharmacology
    |January 1, 1976
    PubMed
    Summary
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    Opiates reduce cyclic AMP (adenosine monophosphate) in rat brains, a key finding for understanding opiate action and withdrawal. This research links cyclic AMP levels to morphine dependence and abstinence symptoms.

    Area of Science:

    • Neuropharmacology
    • Molecular Biology
    • Neuroscience

    Background:

    • Opiates are known to affect neuronal function, but the precise molecular mechanisms underlying their action, particularly concerning cyclic nucleotide signaling, remain incompletely understood.
    • Cyclic AMP (adenosine monophosphate) is a crucial second messenger involved in various cellular processes, including neurotransmission and neuronal plasticity.

    Purpose of the Study:

    • To investigate the effect of opiates on cyclic AMP (adenosine monophosphate) formation in rat brain homogenates.
    • To explore the role of cyclic AMP and cyclic GMP in morphine dependence and abstinence phenomena.
    • To elucidate the relationship between opiate action, neuronal cyclic AMP levels, and the development of abstinence syndromes.

    Main Methods:

    • Measurement of prostaglandin E-stimulated cyclic AMP (adenosine monophosphate) formation in rat brain homogenates.

    Related Experiment Videos

  • Stereospecificity and dose-response studies of opiate effects on cyclic AMP (adenosine monophosphate) levels.
  • Intracerebroventricular administration of cyclic AMP and cyclic GMP in morphine-dependent rats.
  • Administration of xanthines (theophylline, 3-isobutyl-1-methylxanthine) to naive rats and assessment of withdrawal-like symptoms.
  • Inhibition studies of cyclic AMP phosphodiesterase by xanthines in rat brain homogenates.

    • Main Results:

    • Opiates stereospecifically inhibited prostaglandin E-stimulated cyclic AMP (adenosine monophosphate) formation in a dose-dependent manner, correlating with agonist potency.
    • Naloxone antagonized opiate effects without affecting basal cyclic AMP (adenosine monophosphate) levels.
    • Intracerebroventricular cyclic AMP intensified, while cyclic GMP diminished, precipitated abstinence in morphine-dependent rats.
    • Xanthines, known phosphodiesterase inhibitors, induced a quasi-morphine abstinence syndrome in naive rats, which was modulated by heroin and naloxone.

    Conclusions:

    • Opiate agonists likely inhibit an adenylate cyclase in morphine-sensitive neurons, leading to decreased neuronal cyclic AMP (adenosine monophosphate) levels.
    • Both morphine abstinence and the quasi-abstinence syndrome induced by xanthines are associated with an increase in neuronal cyclic AMP (adenosine monophosphate).
    • These findings suggest the existence of two endogenous humoral mediators acting on morphine-sensitive neurons: one morphine-like and one anti-morphine-like.