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Submitted on June 22, 2005
Accepted on July 10, 2006
Centre for Neuroendocrinology and Dept of Anatomy and Structural Biology, University of Otago School of Medical Sciences, PO Box 913, Dunedin 9001, New Zealand
* To whom correspondence should be addressed. E-mail: greg.anderson{at}anatomy.otago.ac.nz.
During late pregnancy and lactation, the tuberoinfundibular dopamine (TIDA) neurons that regulate prolactin secretion by negative feedback become less able to produce dopamine in response to prolactin, leading to hyperprolactinemia. Since prolactin-induced activation of dopamine synthesis in these neurons requires the JAK/STAT5b signaling pathway, we investigated whether prolactin-induced STAT5b signaling is reduced during lactation, and whether induction of suppressors of cytokine signaling (SOCS) mRNAs occur at this time and in late pregnancy. During lactation, the ability of exogenous prolactin to induce STAT5 phosphorylation and STAT5b nuclear translocation was markedly reduced when compared with diestrous rats. In non-pregnant female rats, acute treatment with ovine prolactin markedly increased levels of SOCS-1, -3 and CIS mRNA in arcuate nucleus micropunches. On gestation (G) day 22, SOCS-1 and SOCS-3 mRNA levels were 10-fold than on G20. SOCS-1, -3 and CIS mRNA levels were also elevated on lactation day 7 (L7). At these times dopaminergic activity was decreased and the rats were hyperprolactinaemic. The high levels of SOCS mRNA were prevented by bromocriptine pretreatment (G22) or pup removal (L7), which suppressed circulating prolactin to basal levels. These results demonstrate that around the end of pregnancy prolactin loses the ability to activate STAT5b, associated with an increase in SOCS mRNAs. The loss of this stimulating pathway may underlie the reduced TIDA neuron dopamine output and hyperprolactinaemia that characterizes late pregnancy and lactation. The high maternal levels of SOCS mRNAs appear to be dependent on prolactin, presumably acting through an alternative signaling pathway to STAT5b.
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