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Related Experiment Videos

Experimental tardive dyskinesia.

L M Gunne, J E Häggström

    The Journal of Clinical Psychiatry
    |April 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    Neuroleptic drugs can cause movement disorders by reducing glutamic acid decarboxylase (GAD) activity. Animal models show GAD reduction in specific brain areas is linked to these neuroleptic-induced dyskinesias.

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    Area of Science:

    • Neuroscience
    • Pharmacology

    Background:

    • Chronic neuroleptic administration is associated with movement disorders.
    • Glutamic acid decarboxylase (GAD) is a key enzyme in GABA synthesis.
    • Homovanillic acid (HVA) is a dopamine metabolite.
    • Neuroleptic-induced dyskinesias (NID) are a significant side effect of antipsychotic medications.

    Purpose of the Study:

    • To investigate the regional distribution of GAD and brain HVA levels in animal models of chronic neuroleptic administration.
    • To determine if changes in GAD activity and HVA levels correlate with the development of NID.

    Main Methods:

    • Chronic administration of neuroleptics to Cebus apella monkeys and rats.
    • Measurement of GAD activity in specific brain regions (substantia nigra, medial globus pallidus, nucleus subthalamicus).

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  • Assay of neostriatal HVA levels.

    • Main Results:

    • Reduced GAD activity was observed in the substantia nigra, medial globus pallidus, and nucleus subthalamicus of animals that developed NID.
    • These GAD reductions were not present in animals that did not develop movement disorders.
    • Neostriatal HVA levels were reduced in dyskinetic monkeys.

    Conclusions:

    • Reduced GAD activity in specific brain areas is a potential mechanism underlying NID.
    • Animal models exhibiting these biochemical changes can serve as valuable tools for screening novel antipsychotics.
    • These models may aid in developing strategies to prevent tardive dyskinesia.