CORTICOSTERONE RESPONSE TO THE SEROTONERGIC AGONIST D-FENFLURAMINE MAY BE INDEPENDENT FROM CORTICOTROPIN-RELEASING FACTOR (CRF)

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).