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Related Experiment Videos

Apomorphine increases vesicular monoamine transporter-2 function: implications for neurodegeneration.

Jannine G Truong1, Glen R Hanson, Annette E Fleckenstein

  • 1Department of Pharmacology and Toxicology, University of Utah, 30 South 2000 East, Salt Lake City, UT 84112, USA.

European Journal of Pharmacology
|June 5, 2004
PubMed
Summary

Apomorphine, a Parkinson's disease drug, enhances dopamine uptake by increasing vesicular monoamine transporter-2 (VMAT-2) function. This neuroprotective effect, observed in rats, suggests a novel therapeutic mechanism for neurodegenerative conditions.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Neurodegenerative Diseases

Background:

  • Apomorphine is a dopamine agonist used to treat Parkinson's disease symptoms.
  • Previous research suggests potential neuroprotective effects of apomorphine.
  • Altering vesicular monoamine transporter-2 (VMAT-2) function may protect against dopaminergic degeneration.

Purpose of the Study:

  • To investigate the effect of apomorphine on VMAT-2 function.
  • To determine if apomorphine influences vesicular dopamine uptake.

Main Methods:

  • Apomorphine was administered to rats of different ages (postnatal day 40 and 90).
  • Vesicular dopamine uptake was measured in purified striatal vesicles.
  • VMAT-2 protein redistribution within nerve terminals was analyzed.

Related Experiment Videos

  • The effect of eticlopride, a dopamine D2 receptor antagonist, was assessed.

    • Main Results:

    • Apomorphine rapidly and reversibly increased vesicular dopamine uptake in rat striatal vesicles.
    • This effect was observed in both young and adult rats.
    • Apomorphine treatment led to a redistribution of VMAT-2 protein in nerve terminals.
    • The apomorphine-induced increase in dopamine uptake was blocked by eticlopride.

    Conclusions:

    • Apomorphine enhances VMAT-2 function, increasing vesicular dopamine uptake.
    • This action is mediated through dopamine D2 receptors.
    • Findings suggest a novel mechanism for apomorphine's potential neuroprotective effects in neurodegenerative diseases.