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).
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