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Evaluating prolactin response to dopamine agonists in schizophrenia. Methodological problems.

B M Davis, K L Davis, R C Mohs

    Archives of General Psychiatry
    |March 1, 1985
    PubMed
    Summary
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    Serum prolactin levels in schizophrenic patients did not decrease as much as in healthy individuals after apomorphine challenge. This suggests a potential difference in dopamine receptor sensitivity in schizophrenia.

    Area of Science:

    • Neuroendocrinology
    • Psychiatry
    • Pharmacology

    Background:

    • Altered prolactin (PRL) regulation is observed in chronic schizophrenia.
    • Dopamine agonists are used to challenge the pituitary-adrenal axis and assess PRL secretion.

    Purpose of the Study:

    • To investigate serum prolactin responses to dopamine agonists in chronic schizophrenic subjects compared to controls.
    • To determine if illness state (exacerbation vs. remission) affects prolactin levels.

    Main Methods:

    • Serum PRL levels were measured in 19 controls and 38 schizophrenic patients after challenges with apomorphine, saline, dopamine, or levodopa-carbidopa.
    • Baseline PRL levels were correlated with age and subsequent PRL measurements.
    • Percent decrease in PRL after drug administration was analyzed as a measure of drug response.

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    Main Results:

    • Baseline PRL levels showed an inverse relationship with age.
    • Percent PRL decrease after apomorphine was significantly greater in normal subjects than in schizophrenics.
    • When apomorphine responses were corrected for placebo effects, the difference between groups was eliminated.
    • No significant differences in PRL response were observed between dopamine and levodopa-carbidopa challenges.

    Conclusions:

    • The blunted prolactin response to apomorphine in schizophrenics may be due to placebo effects or altered dopamine receptor function.
    • Illness exacerbation was associated with lower baseline PRL levels in patients.
    • Further research is needed to clarify the role of dopamine pathways in schizophrenia-related PRL dysregulation.