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Related Experiment Videos

Naloxone enhances motion sickness: endorphins implicated.

M E Allen, C McKay, D M Eaves

    Aviation, Space, and Environmental Medicine
    |July 1, 1986
    PubMed
    Summary
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    Naloxone administration accelerated motion sickness onset and prolonged discomfort compared to placebo, suggesting endogenous opiates play a protective role. This research explores the link between opioid withdrawal, neuron hypersensitivity, and susceptibility to motion sickness.

    Area of Science:

    • Neuroscience
    • Human Physiology
    • Pharmacology

    Background:

    • Motion sickness is a common condition affecting human subjects exposed to specific motion stimuli.
    • The role of endogenous opioid systems in the modulation of motion sickness has not been fully elucidated.

    Purpose of the Study:

    • To investigate the effect of naloxone, an opioid antagonist, on the development and duration of motion sickness.
    • To explore the potential involvement of endogenous opiates in the body's protective or adaptive responses to motion stress.

    Main Methods:

    • A double-blind, cross-over study design was employed.
    • Human subjects were exposed to Coriolis stimulation in a rotating chair.
    • Naloxone and placebo were administered to evaluate their impact on motion sickness progression.

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    Main Results:

    • Subjects receiving naloxone reached the Malaise III sickness level significantly faster than those receiving placebo.
    • Discomfort persisted for up to 3 days after naloxone administration, a prolonged effect not observed with placebo.
    • These findings suggest a significant role for endogenous opiates in mitigating motion sickness.

    Conclusions:

    • Endogenous opiates appear to possess an endogenous protective or adaptive function in controlling motion sickness.
    • Endogenous opioid withdrawal, potentially post-exercise, may induce neuron hypersensitivity, increasing susceptibility to emetic stimuli.
    • Elevated endorphin levels may confer greater tolerance to motion stress by preventing withdrawal-induced hypersensitivity.