Evidence that a Serotonergic Mechanism Stimulates the Secretion of Pituitary β-Endorphin-Like Immunoreactivity in the Rat*

Publisher Website
Google Scholar
Abstract
A pharmacological approach was used to investigate serotonergic control of the secretion of pituitary β-endorphin- like immunoreactivity (β-END-LI) in the rat. The administration of 75 or 200 mg/kg L-tryptophan (ip, over 30 min) increased brain serotonin by 17% and 19%, respectively, and increased circulating β-END-LI from 0.30 ± 0.6 to 0.56 ±0.7 and 0.64 ± 0.8 ng/ml, respectively. D,L,5-Hydroxytryptophan (30 mg/kg, ip, over 30 min) produced a 4.9-fold increase in brain serotonin content and a 3.4-fold rise in plasma β-END-LI. The administration of a serotonin reuptake blocker, fluoxetine (10 mg/kg, ip, over 15 min), elevated basal levels of plasma β-ENDLI from a control value of 0.38 ± 0.02 to 1.21 ± 0.32 ng/ml. Exposure to ether increased circulating β-END-LI to 1.08 ± 0.18 ng/ml, and fluoxetine treatment further increased this rise to 1.69 ± 0.09 ng/ml (P < 0.05). Quipazine, a serotonin receptor agonist, evoked a dose-related (2.5-5.0 mg/kg, ip) increase in circulating β-END-LI levels by 15–45 min post injection. By contrast, intraventricular injection of the neurotoxin 5,7-dihydroxytryptamine (75 jug free base, for 10 days) caused a 77% depletion of brain serotonin and attenuated the rise in β-END-LI levels in response to immobilization (3.28 ± 0.20 vs. 1.83 ± 0.25 ng/ml). A higher dose of 5,7-dihydroxytryptamine (200 jug free base, for 10 days) significantly decreased resting levels of 0-END-LI from 0.65 ± 0.14 to 0.36 ± 0.08 ng/ml. We conclude that brain serotonin neurons exert a stimulatory influence over the basal secretion of pituitary β-END-LI and mediate, in part, the stress-induced release of this hormone.