Unlike other anterior pituitary hormones, prolactin release is regulated via tonic inhibition by prolactin-inhibitory factor (PIF), which was later determined to be dopamine. Dopamine neurons in the tuberoinfundibular system of the hypothalamus directly inhibit prolactin release. Prolactin can also inhibit its own release by a short-loop negative feedback to the hypothalamus. TRH, oxytocin, serotonin, oestrogen and other neuroregula-tors also have prolactin-releasing factor activity . Prolactin primarily regulates the behavioural aspects of reproduction and infant care. Basal prolactin levels increase in females following parturition, and suckling stimulates prolactin release. Prolactin itself stimulates breast growth and milk synthesis.
Excess circulating prolactin can lead to a number of clinical symptoms. Hyperprolactinemia often leads to reduced testosterone secretion in men and a decreased libido in both men and women. Patients may also complain of depression, stress intolerance, anxiety and increased irritability, which usually resolve following treatments that reduce serum prolactin levels. Despite these effects, alterations in the hypothalamic-prolactin axis have not been clearly demonstrated in psychiatric disorders . Hyperprolac-tinemia also frequently occurs following treatment with conventional anti-psychotic medications, because of their potent blockade of dopamine receptors. Because prolactin release is inhibited by dopamine, the prolactin response to infusions of dopaminergic agonists has also been used to estimate CNS dopaminergic tone, though it probably only reflects hypothal-amic dopamine neuronal function.
Although abnormalities in prolactin secretion have not been clearly demonstrated in depression per se, a large number of reports have used provocative tests of prolactin secretion in patients with psychiatric disorders (for a review see ). Briefly, these tests use agents that increase serotonergic transmission, for example l-tryptophan, 5-hydroxytryptophan (5HTP), and fenfluramine, among others. In general, the prolactin response to agents that increase serotonergic activity is blunted in depression [113, 114], as well as in patients with cluster B personality disorders . These data suggest that the blunted prolactin response is mediated by alteration in 5HTiA receptor responsiveness, and that serotonergic transmission in these patients is abnormal.
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