Corticosterone response to the serotonergic agonist d-fenfluramine may be independent from corticotropin-releasing factor (CRF)

https://doi.org/10.1016/0304-3940(93)90454-SGet rights and content

Abstract

This study was designed to assess the involvement of corticotropin-releasing factor (CRF) in the corticosterone response to the acute administration of the serotonergic indirect agonist d-fenfluramine in the rat. In addition to plasma corticosterone, d-fenfluramine-induced hyperglycemia (which is independent from the hypothalamo-pituitary-adrenal axis) was also analyzed. Acute i.v. injection of sheep anti-CRF antiserum (15 min beforehand) markedly diminished ether stress-induced corticosterone release (but not ether stress-induced increases in plasma glucose levels), thereby indicating that passive immunization was efficient. Acute administration of d-fenfluramine (3 mg/kg i.v.) increased plasma corticosterone and glucose levels to similar extents in control rats (i.e. injected with normal sheep serum) and in anti-CRF antiserum-injected rats. These results indicate that, under our experimental conditions, d-fenfluramine-induced corticosterone elevation is of peripheral origin (through pituitary and/or adrenocortical pathways).

References (20)

There are more references available in the full text version of this article.

Cited by (7)

  • Serotonin and hippocampal neurogenesis

    1999, Neuropsychopharmacology
View all citing articles on Scopus
View full text