Prolactin suckling

The function of oxytocin is to cause uterine contraction and the release of milk from the mammary glands. As with prolactin, suckling, via the neural pathways, induces oxytocin secretion by the neurohypophysis. Blood oxytocin levels increase greatly just before parturition. Oxytocin is used as a drug to induce labor in pregnant women at term. 

The release of prolactin from the adenohypophysis is normally inhibited by prolactin-inhibiting hormone (PIH, dopamine) from the hypothalamus. Prolactin secretion is also controlled by prolactin-releasing factor (PRF). The release of PRF from the hypothalamus is mediated by reflexes elicited by suckling and breast stimulation. 

Maternal prolactin via the milk is required for normal development of the tuberoinfundibular neuronal system of the hypothalamus during the neonatal period in rats (Shyr et al., 1986). Blocking the suckling-induced rise in maternal prolactin levels causes abnormal tuberoinfundibular function, with decreased inhibition by dopamine of prolactin secretion in the offspring later in life. The resulting chronically elevated prolactin levels cause prostatitis in the male offspring (Tangbanluekal Robinette, 1993). 

The herbicide atrazine suppresses pituitary prolactin secretion in adult rats and suppresses suckling-induced increases in prolactin secretion in lactating rats by stimulating hypothalamic dopamine secretion (Stoker et al., 1999 Cooper et al., 2000). By altering prolactin secretion in the mother, atrazine exposure during lactation causes elevated prolactin levels in the male offspring at puberty (Stoker et al., 1999). Subsequently, these males develop persistent inflammatory changes in the lateral prostate (Stoker et al., 1999). 

Stoker TE, Robinette CL, Cooper RL (1999) Maternal exposure to atrazine during lactation suppresses suckling-induced prolactin release and results in prostatitis in the adult offspring. Toxicol Sci, 52 68-79. 

Figure 16.3 Short feedback loop controlling prolactin (PRL) secretion. PRL secretion by the anterior pituitary is normally inhibited by the PRL inhibiting factor (PIF) secreted by hypothalamus. PIF is dopamine. The suckling reflex stops PIF secretion and allows the pituitary to produce and export prolactin. Accumulation of PRL in the pituitary causes its backup through a portal vein into the hypothalamus, eliciting a derepression of PIF production and a subsequent decrease in PRL export.

Baumann MH, Rabii J (1991) Inhibition of suckling-induced prolactin release by p- and K-opioid antagonists. Brain Res 567 224-230. 

Callahan P, Klosterman S, Prunty D, Tompkins J, Janik J (2000) Immunoneutralization of endogenous opioid peptides prevents the suckling-induced prolactin increase and the inhibition of tuberoinfundibular dopaminergic neurons. Neuroendocrinology 77 268-276. 

Jacobowitz R, Callahan P, Janik, J (1997) Immunoneutralization of P-endorphin blocks prolactin release during suckling without affecting tuberoinfundibular dopaminergic neural activity. Life Sci 67 1301 1311. 

Pape J-R, Ciofi P, Tramu G (1996) Suckling-induced Fos-immunoreactivity in subgroups of hypothalamic POMC neurons of the lactating rat investigation of a role for prolactin. J Neuroendocrinol 8 375-386. 

Selmanoff MK, Gregerson KA (1986) Suckling-induced prolactin release is suppressed by naloxone and stimulated by P-endorphin. Neuroendocrinology 42 255-259. 

Prolactin, produced in response to suckling of an infant, stimulates the synthesis of milk proteins during lactation. 

L-tryptophan and serotonin are powerful releasers of prolactin and have been shown to be involved in some physiological states in which prolactin is released, i.e., during suckling, stress, etc.83 Hypothalamic regulations of prolactin secretion in animals (mammals) and humans have been reported to be similar. 

Released from the hypothalamus in response to suckling brings about release of prolactin. 

Oxytocin is synthesized in the cell bodies of supraoptic and paraventricular neurons and, then, transported (complexed with neurophysin) in membrane-bound vesicles to the posterior lobe of the pituitary gland, where it may be released by a reflex mechanism or mechanisms, initiated or amplified by genital stimulation, coitus, parturition, or suckling of the infant. Suckling also releases prolactin. The action of oxytocin on the uterus (muscular contraction and parturition) and mammary glands (contraction of myoepithelial cells and milk secretion) is a direct one and is not influenced by the autonomic nervous system. 

Tyrey, L. and Hughes, C.L. (1984) Inhibition of suckling-induced prolactin secretion by delta-9-tetrahydrocannabinol, in The Cannabinoids Chemical, Pharmacologic and Therapeutic Aspects, S. Agurell, W.L. Dewey, and R.E. Wilette, lids., pp. 487-495, San Diego, CA Academic Press. 

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