Control of prolactin secretion

Abstract

1. Prolactin is a 21,500 Dalton single-chain polypeptide hormone but may occur in 50 kDa and 150 kDa molecular variants. 2. These large PRL variants may be secreted predominantly; this condition is termed "macroprolactinemia". It is characterized by high immunological and normal biological serum levels of prolactin, and lack of clinical symptoms of hyperprolactinemia. 3. The information on PRL is encoded on chromosome 6. Transcription can be enhanced and suppressed by a variety of hormonal factors. 4. PRL is secreted in a pulsatile fashion; it displays a circadian rhythm (with a maximum during sleep) and is stimulated by some amino acids. PRL also responds to mechanical stimulation of the breast. 5. PRL rises during pregnancy, and maintainance of hyperprolactinemia (and, thereby, physiological infertility) is dependent on the frequency and duration of breast feedings. 6. Hypothalamic regulation of prolactin mainly involves tonic inhibition via portal dopamine. The physiological importance of various stimulating factors present in the hypothalamus is still incompletely understood. In particular, there is still no place for TRH in PRL physiology. 7. PRL is released in response to stress; this response may be mediated by opioids. The low-estrogen, low-gonadotropin amenorrhea of endurance-training women is not mediated by prolactin, however. 8. Estrogens stimulate PRL gene transcription via at least two independent mechanisms. There are many clinical examples of this estrogen effect on prolactin serum levels, and also on the growth of prolactinomas. 9. Mild hyperprolactinemia remains an enigma which cannot satisfactorily be resolved by biochemical or radiological testing. The border between "normal" and "elevated" prolactin is ill-defined. The possibility of macroprolactinemia complicates this matter even further. 10. The number of drugs which suppress prolactin by acting on pituitary D2 receptors, and which are useful in the treatment of hyperprolactinemia, continues to increase. In the field of ergot alkaloids, parenteral application appears to be a logical solution to the problem of the high first-pass effect; in addition, this form of treatment is frequently better tolerated than the oral route. 11. Prolactinoma development is presently being studied employing molecular biological techniques; the question of whether tumorigenesis can be attributed to specific defects of gene regulation remains to be answered.

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

“…Besides stimulating the secretion of PRL in vivo and in vitro, TRH has also been shown to stimulate PRL gene expression (Benker et al, 1990). TRH binds to membrane receptors on the lactotrophs, activating the phospholipase C signaling pathway (Bjoro et al, 1990).…”

“…TRH binds to membrane receptors on the lactotrophs, activating the phospholipase C signaling pathway (Bjoro et al, 1990). This pathway culminates in the activation of protein kinase C, with consequent increased PRL gene expression (Benker et al, 1990).…”

“…In addition to its direct actions on PRL gene expression, estrogen also interacts with PRFs at the hypothalamic level (Benker et al, 1990). Estrogen treatment stimulates PRL release by influencing hypothalamic VIP (Lam et al, 1990), and also OT gene expression (Shughrue et al, 2002).…”

Endocrine and immunologic markers in manganese alloy production workers

“…Hence, the results do not, in our opinion, provide enough evidence to suggest that exposure to manganese influences the serum concentration of LH. It has, however, been described that an increased serum prolactin concentration may result in increased central dopaminergic tone, which could result in a loss of LH pulsatility (20). This possibility suggests that sufficiently high exposure may alter LH.…”

Establishment of Reference Interval of Serum Prolactin in an Indian Population

“…Human prolactin is secreted from the anterior pituitary gland in both male and female. The release and synthesis of prolactin is episodic and is under neuroendocrinal control mainly through prolactin releasing factor and prolactin inhibiting factor [3]. There are mainly three different forms of prolactin of which the little prolactin (22-kDa) is the biological active form [4,5].…”