Neuroendocrine mechanisms underlying the control of gonadotropin secretion by steroids

Virendra B. Mahesh, Darrell W. Brann

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

There is considerable evidence that although estradiol may trigger the preovulatory surge of gonadotropins, progesterone is required for its full magnitude and duration and that glucocorticoids bring about selective follicle-stimulating hormone release. The luteinizing hormone-releasing hormone (LHRH) neuron does not have steroid receptors and is regulated by excitatory amino acid neurotransmission. Steroids do not appear to modulate excitatory amino acid receptors directly but increase release of glutamate in the preoptic area. This may be due to the suppression by steroids of the enzyme glutamatic acid decarboxylase67 that converts glutamate into GABA. NMDA receptors colocalize with nitric oxide synthase-containing neurons that surround the LHRH neurons in the preoptic area and intersect the LHRH fibers in the median eminence. Other potential novel pathways of LHRH release that are currently being explored include carbon monoxide generated by the action of heme oxygenase-2 on heme molecules and bradykinin acting via bradykinin B2 receptors.

Original languageEnglish (US)
Pages (from-to)252-256
Number of pages5
JournalSteroids
Volume63
Issue number5-6
DOIs
Publication statusPublished - May 1 1998

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Keywords

  • Bradykinin
  • Carbon monoxide
  • Excitatory amino acids
  • LH
  • LHRH
  • Nitric oxide

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology
  • Pharmacology
  • Clinical Biochemistry
  • Organic Chemistry

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