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Related Experiment Videos

Abnormal dopamine sensitivity in some human prolactinomas.

I Pellegrini1, R Costa, F Grisoli

  • 1Laboratoire de Neuroendocrinologie Expérimentale, Faculté de Médecine Nord, INSERM U 297, Marseille, France.

Hormone Research
|January 1, 1989
PubMed
Summary
This summary is machine-generated.

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Some patients with prolactin (PRL)-secreting adenomas are resistant to bromocriptine. This resistance may stem from defects in dopamine receptor signaling or post-receptor pathways.

Area of Science:

  • Endocrinology
  • Molecular Endocrinology
  • Pituitary Disorders

Background:

  • Dopamine agonists, like bromocriptine, typically suppress prolactin (PRL) secretion in human prolactin-secreting adenomas.
  • A subset of patients exhibits resistance to bromocriptine, necessitating further investigation into underlying mechanisms.

Purpose of the Study:

  • To investigate the cellular mechanisms of bromocriptine resistance in a cohort of patients with prolactin-secreting adenomas.
  • To compare the response of adenoma cells to bromocriptine with that of normal pituitary cells.

Main Methods:

  • Primary cultures of human prolactin-secreting adenoma cells from six resistant patients were established.
  • In vitro studies assessed the effects of bromocriptine, sulpiride, cholera toxin, and pertussis toxin on PRL release.

Related Experiment Videos

  • Inhibition percentages of PRL release were quantified and compared between adenoma and normal pituitary cells.

    • Main Results:

    • Bromocriptine demonstrated significantly reduced inhibition of PRL release in adenoma cells (32%) compared to normal pituitary cells (65%).
    • Sulpiride partially reversed the inhibitory effect of bromocriptine, suggesting involvement of dopamine receptors.
    • Bacterial toxins modulated bromocriptine's efficacy, indicating potential post-receptor signaling pathway defects.

    Conclusions:

    • Patients with bromocriptine-resistant prolactinomas may possess cellular defects affecting dopamine receptor signaling or downstream pathways.
    • These findings highlight the complexity of dopamine agonist resistance and suggest potential targets for future therapeutic strategies.