Central opioid activity in polycystic ovary syndrome with and without dopaminergic modulation

Randall B. Barnes, Rogerio A. Lobo*

*Corresponding author for this work

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

It has been hypothesized that brain opioid activity may be decreased in patients with the polycystic ovary syndrome (PCO) and that this decrease may, in part, explain the elevated levels of LH characteristic of the syndrome. We, therefore, examined the LH and PRL responses to naloxone infusions (2 mg/h for 4 h) in seven women with PCO and five weight- and estrogen-matched normal women. The infusions were given both before and after pretreatment with L-dopacarbidopa (L-DOPA-C) because dopaminergic activity may be decreased in PCO, and dopamine may interact with the brain opioid system. Both PCO patients and normal women had similar responses of serum LH during naloxone treatment; the mean maximum LH responses were 53 ± 15% (±SE) in normal women and 51 ± 12% in PCO patients (P > 0.05). PRL levels were also unaffected by naloxone infusion. After L-DOPA-C pretreatment, baseline LH and PRL levels were unchanged in normal women and PCO patients, and the naloxone-induced LH rise was completely abolished in the normal women. However, in PCO patients, LH increased from 24.7 ± 4 to 31 ± 5 mlU/ml, with a mean maximum increase of 112 ± 33% during naloxone infusion (P < 0.05). We conclude that 1) brain or central opioid activity is not decreased in PCO; 2) increased central opioid activity does not appear to be responsible for the increased LH levels characteristic of the syndrome; and 3) decreased central dopamine activity and/or the interaction between the dopaminergic and opioid systems may be altered in PCO.(J Clin Endocrinol Metab 61 : 779, 1985).

Original languageEnglish (US)
Pages (from-to)779-782
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume61
Issue number4
DOIs
StatePublished - Oct 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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