Dexamethasone facilitates release of the neuropeptide α-MSH

Anna Catania, Leigh W. Martin, James M. Lipton

Research output: Contribution to journalArticlepeer-review


α-Melanocyte stimulating hormone (α-MSH) has important host defense properties, in part similar to those of corticosteroids. Previous research suggests that secretion of α-MSH and of ACTH are controlled separately. The relationship between release of α-MSH and the activity of the hypothalamic-pituitary-adrenal axis in the rabbit was examined by monitoring changes in circulating α-MSH, ACTH, and corticosterone in response to endotoxin and corticotropin-releasing hormone (CRH), both with and without dexamethasone pretreatment. Endotoxin (1 μg/kg IV) did not cause α-MSH release, but it did increase plasma concentrations of ACTH and corticosterone. Similarly, CRH (1 and 10 μg/kg IV) did not affect plasma α-MSH, whereas it stimulated ACTH and corticosterone release. Dexamethasone pretreatment abolished the responses of ACTH and corticosterone to either stimulus and did not modify circulating α-MSH after CRH. In contrast, dexamethasone pretreatment did result in a significant increase in plasma α-MSH after a dose of endotoxin that was ineffective alone. These data indicate that corticosteroids can facilitate the release of α-MSH, a powerful anti-inflammatory hormone. Since corticosteroids are released with certain challenges, this facilitatory activity may be important to the host response.

Original languageEnglish
Pages (from-to)727-730
Number of pages4
JournalBrain Research Bulletin
Issue number5
Publication statusPublished - 1991


  • ACTH
  • Corticotropin-releasing hormone
  • Endotoxin
  • α-MSH

ASJC Scopus subject areas

  • Neuroscience(all)


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