Crowding stress inhibits serotonin 1A receptor-mediated increases in corticotropin-releasing factor mRNA expression and adrenocorticotropin hormone secretion in the Gulf toadfish

Lea R. Medeiros, Maria C. Cartolano, M. Danielle McDonald

Research output: Contribution to journalArticle

9 Scopus citations


Stimulation of the serotonin 1A (5-HT1A) receptor subtype by 5-HT has been shown to result in an elevation in plasma corticosteroid levels in both mammals and several species of teleost fish, including the Gulf toadfish (Opsanus beta); however, in the case of teleost fish, it is not clearly known at which level of the hypothalamic-pituitary-interrenal axis the 5-HT1A receptor is stimulated. Additionally, previous investigations have revealed that chronic elevations of plasma cortisol mediate changes in brain 5-HT1A receptor mRNA and protein levels via the glucocorticoid receptor (GR); thus, we hypothesized that the function of centrally activated 5-HT1A receptors is reduced or abolished as a result of chronically elevated plasma cortisol levels and that this response is GR mediated. Our results are the first to demonstrate that intravenous injection of the 5-HT1A receptor agonist, 8-OH-DPAT, stimulates a significant increase in corticotropin-releasing factor (CRF) precursor mRNA expression in the hypothalamic region and the release of adrenocorticotropic hormone (ACTH) from the pituitary of teleost fish compared to saline-injected controls. We also provide evidence that cortisol, acting via GRs, attenuates the 5-HT1A receptor-mediated secretion of both CRF and ACTH.

Original languageEnglish (US)
Pages (from-to)259-271
Number of pages13
JournalJournal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology
Issue number2
StatePublished - Feb 1 2014



  • 8-OH-DPAT
  • Antalarmin
  • Hypothalamic-pituitary-interrenal (HPI) axis
  • RU486
  • Stress

ASJC Scopus subject areas

  • Physiology
  • Ecology, Evolution, Behavior and Systematics
  • Animal Science and Zoology
  • Biochemistry
  • Endocrinology

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