Prolactin is a protein hormone of the anterior pituitary gland that was originally named for its ability to promote lactation in response to the suckling stimulus of hungry young mammals. We now know that prolactin is not as simple as originally described. Indeed, chemically, prolactin appears in a multiplicity of posttranslational forms ranging from size variants to chemical modifications such as phosphorylation or glycosylation. It is not only synthesized in the pituitary gland, as originally described, but also within the central nervous system, the immune system, the uterus and its associated tissues of conception, and even the mammary gland itself. Moreover, its biological actions are not limited solely to reproduction because it has been shown to control a variety of behaviors and even play a role in homeostasis. Prolactin-releasing stimuli not only include the nursing stimulus, but light, audition, olfaction, and stress can serve a stimulatory role. Finally, although it is well known that dopamine of hypothalamic origin provides inhibitory control over the secretion of prolactin, other factors within the brain, pituitary gland, and peripheral organs have been shown to inhibit or stimulate prolactin secretion as well. It is the purpose of this review to provide a comprehensive survey of our current understanding of prolactin's function and its regulation and to expose some of the controversies still existing.

/pdf/prolactin-structure-function-and-regulation-of-secretion-3w4x6fqbg3.pdf

Prolactin: Structure, Function, and Regulation of Secretion

Since the isolation of the enkephalins five yr ago, there has been an explosive increase in knowledge concerning the effects of the opiates and opioid peptides. This review deals with the interactions of opiates with the endocrine system in rat and man. The opioid peptides have been demonstrated to exert a variety of effects on pituitary hormone secretion in rat and man. In the rat, opiates stimulate growth hormone, prolactin and ACTH release and inhibit the release of the glycoprotein hormones. In man, the physiologic role of the endogenous opiates appears to be involved predominantly in ACTH and gonadotrophin regulation. Opiate effects are mainly exerted at the level of the hypothalamus but further modulating effects may occur at the pituitary and at end-organs. Opiate-induced hormonal effects appear to be mediated through dopaminergic and/or serotonergic mechanisms. Recent studies have also suggested a possible local neuromodulatory role for the opioid peptides in the control of carbohydrate metabolism and reproductive processes.

The endocrinology of the opiates and opioid peptides

Morphine- and opioid peptide-induced inhibition of the release of dopamine from tuberoinfundibular neurons

I. Introduction IN THE RAT, the corpus luteum is formed on the morning of estrus in response to the surge of luteinizing hormone released on the previous day, proestrus. However, unlike other mammals whose corpora lutea secrete increasing amounts of progesterone for several days (1), the newly formed corpora lutea of the rat secrete progesterone for only 2 days after formation (2, 3). In the absence of all other input, the corpora lutea subsequently fail and progesterone secretion wanes (3). It has long been appreciated that rodent corpora lutea could be maintained by either coital stimulation (4) or injection of pituitary extracts containing prolactin (PRL) activity (5, 6). An overwhelming literature now indicates that the mating stimulus induces the release of PRL which in turn “rescues” the corpora lutea of the cycle and prolongs the ability of these structures to secrete progesterone (3, 7–11). The mating stimulus or copulomimetic stimuli applied to the uterine cervix with a glass rod or appropriately...

The mating-induced release of prolactin: a unique neuroendocrine response.

Light- and electron-microscopic immunocytochemistry of glutamic acid decarboxylase (GAD) in the basal hypothalamus: morphological evidence for neuroendocrine gamma-aminobutyrate (GABA).

gamma-Aminobutyric acid (GABA) inhibits PRL release from incubated hemipituitaries in a dose-dependent manner. The maximum inhibition obtained with GABA is less than that obtained with dopamine. Its affinity is 100 times lower. The effect is blocked by picrotoxin but not by a dopamine inhibitor; alpha-flupentixol but not picrotoxin antagonizes dopamine inhibition. This indicates that dopamine and GABA inhibit PRL release through independent receptors. The hypothalamic extract contains sufficient GABA to inhibit PRL release in our in vitro conditions. Picrotoxin, however, does not significantly inhibit the nondopaminergic PRL-inhibiting activity of mediobasal hypothalamic extracts. Another nondopaminergic PRL-inhibiting factor, therefore, seems to be present in the hypothalamus.

Independent Inhibition of Prolactin Secretion by Dopamine and γ-Aminobutyric Acid in Vitro

Effect of morphine on the dopamine inhibition of pituitary prolactin release in vitro.

[Dopamine, GABA-PIF and in vitro regulation of prolactin secretion in the rat (proceedings) (author's transl)].

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Independent Inhibition of Prolactin Secretion by Dopamine and γ-Aminobutyric Acid in Vitro

Effect of morphine on the dopamine inhibition of pituitary prolactin release in vitro.

[Dopamine, GABA-PIF and in vitro regulation of prolactin secretion in the rat (proceedings) (author's transl)].