Related Experiment Videos
Morphine can stimulate prolactin release independent of a dopaminergic mechanism
S H Shin1, M C Obonsawin, D A Van Vugt
1Department of Physiology, Queen's University, Kingston, Ont., Canada.
Abstract:
Prolactin release is controlled by prolactin-release inhibiting factor (PIF), possibly dopamine, and an unidentified putative hypothalamic prolactin-releasing factor (PRF). Morphine and related opioids may indirectly stimulate prolactin release by inhibiting PIF release and (or) by stimulating putative PRF release. In the present study, we have completely blocked the dopaminergic receptors in normal male rats by pretreatment with a large dose of pimozide (3 mg/kg) to demonstrate if putative PRF has a role in morphine-induced prolactin release. Morphine sulfate (10 mg/kg) was still able to stimulate prolactin release in the rat without any functional dopaminergic PIF receptors. When naloxone (3 mg/kg) was injected 20 min before the morphine in the pimozide-treated rat, plasma prolactin concentration was not affected by morphine indicating that the stimulatory effect of this opioid on prolactin release in the pimozide-pretreated rat was mediated by mu-receptors. We can conclude that morphine can stimulate prolactin release through a mechanism apparently independent of dopaminergic receptors, one possible route being through a putative PRF.
Insights
Morphine stimulates prolactin release independently of dopamine by acting on prolactin-releasing factor (PRF) pathways. This opioid effect is mediated by mu-receptors, not dopaminergic receptors, in male rats.
Area of Science:
- Neuroendocrinology
- Pharmacology
Background:
- Prolactin release is regulated by prolactin-release inhibiting factor (PIF), potentially dopamine, and a putative prolactin-releasing factor (PRF).
- Opioids like morphine may influence prolactin release by modulating PIF and/or PRF pathways.
Purpose of the Study:
- To investigate the role of the putative PRF in morphine-induced prolactin release.
- To determine if dopamine pathways are essential for morphine's effect on prolactin.
Main Methods:
- Normal male rats were pretreated with pimozide to block dopaminergic receptors.
- Morphine sulfate was administered to assess prolactin release.
- Naloxone was used to identify the receptor subtype involved.
Main Results:
- Morphine sulfate stimulated prolactin release even after complete blockade of dopaminergic receptors.
- Naloxone pretreatment blocked the prolactin-releasing effect of morphine, indicating mu-receptor involvement.
- These findings suggest a PRF-mediated mechanism independent of dopamine.
Conclusions:
- Morphine stimulates prolactin release via a mechanism independent of dopaminergic receptors.
- The putative PRF pathway is likely involved in mediating the prolactin-releasing effects of morphine.
- Opioid-induced prolactin release in this context is primarily mediated by mu-receptors.