Elevation of plasma corticosterone by swim stress and insulin-induced hypoglycemia in control and fluoxetine-pretreated rats.
Fluoxetine, a drug that inhibits serotonin inactivation by reuptake from the synaptic cleft and thereby enhances serotonin nerve function, was used to study the possible role of serotonin neurons in the activation of the pituitary-adrenal system of rats by swim stress or insulin-induced hypoglycemia. Fluoxetine pretreatment enhanced the elevation of plasma corticosterone produced by injection of L-5-hydroxytryptophan but did not significantly alter the elevation of plasma corticosterone by swim stress or by insulin-induced hypoglycemia, even when the stimulus was shown to be submaximal. The results suggest that serotonin neural pathways postulated to stimulate ACTH secretion are not involved in the activation of adrenocortical function by these stimuli.
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000097:blood*; D007003:Hypoglycemia / Q000097:blood* / Q000139:chemically induced; D007328:Insulin; D008297:Male; D010647:Phenyl Ethers / Q000494:pharmacology*; D011437:Propylamines / Q000494:pharmacology*; D051381:Rats; D013312:Stress, Physiological / Q000503:physiopathology*; D013550:Swimming; D013997:Time Factors
D007328:Insulin; D010647:Phenyl Ethers; D011437:Propylamines; D006916:5-Hydroxytryptophan; D003345:Corticosterone