Prolactin maintains transient melanin‐concentrating hormone expression in the medial preoptic area during established lactation

Abstract

A population of neurones in the medial part of the medial preoptic area (mPOA) transiently express melanin‐concentrating hormone (MCH) in mid to late lactation in the rat, and this expression disappears on weaning. Prolactin is known to mediate many of the physiological adaptations that occur within the dam associated with lactation and the mPOA is well endowed with prolactin receptors (Prlr); hence, we hypothesised that these transiently MCH‐expressing cells may be regulated by prolactin. By in situ hybridisation, we show that approximately 60% of the cells expressing prepro‐MCH (Pmch) mRNA in the medial part of the mPOA on day 19 of lactation also express Prlr mRNA. To demonstrate that these transiently MCH‐expressing cells can acutely respond to prolactin, dams were treated with bromocriptine on the morning of day 19 of lactation and then given vehicle or prolactin 4 hours later. In the prolactin‐treated animals, over 80% of the MCH‐immunopositive cells were also immunopositive for phosphorylated signal transducer and activator of transcription 5, an indicator of prolactin receptor activation: double immunopositive cells were rare in vehicle‐treated animals. Finally, the effect of manipulating the circulating concentrations of prolactin on days 17, 18 and 19 on the number of MCH‐immunopositive cells on day 19 was determined. Reducing circulating concentrations of prolactin over days 17, 18 and 19 of lactation with or without a suckling stimulus resulted in a reduction (P < 0.05) in the number of MCH‐immunopositive cells in the medial part of the mPOA on day 19 of lactation. Further research is required to determine the functional role(s) of these prolactin‐activated transiently MCH‐expressing neurones; however, we suggest the most likely role involves adaptations in maternal metabolism to support the final week of lactation.

Neuroendocrine control of brown adipocyte function by prolactin and growth hormone

“…Mch (ppMch) mRNA in the medial part of the mPOA also express Prlr by in situ hybridization (Figure 1B). 165 Even so, different timings in MCH increase in POA and Ucp1 decrease in BAT suggest caution in interpreting results. In rats, ppMch mRNA and MCH in POA start to increase on day 8 with highest expression on days 15-21 of lactation, 166 while in mice Ucp1 BAT decrease was evidenced from day 1 of lactation.…”

“…POA neurons expressing Prlr form a complex prolactinresponsive neural circuit, and projections of medial POA Prlr neurons have been traced to several hypothalamic areas crucial to thermogenesis control such as VMN, ARN and PVN. 163 Neurons expressing the MCH can be transiently found in the medial mPOA during lactation, 164,165 and approximately 90% of these colocalise with prolactin-induced phosphorylated signal transducer and activator of transcription 5, and 60% of cells expressing prepro-…”

“…Neurons expressing the MCH can be transiently found in the medial mPOA during lactation, 164,165 and approximately 90% of these colocalise with prolactin‐induced phosphorylated signal transducer and activator of transcription 5, and 60% of cells expressing prepro‐ Mch ( ppMch ) mRNA in the medial part of the mPOA also express Prlr by in situ hybridization (Figure 1B). 165 Even so, different timings in MCH increase in POA and Ucp1 decrease in BAT suggest caution in interpreting results. In rats, ppMch mRNA and MCH in POA start to increase on day 8 with highest expression on days 15–21 of lactation, 166 while in mice Ucp1 BAT decrease was evidenced from day 1 of lactation 167 …”

Sex differences and sex-specific regulation of motivated behavior by Melanin-concentrating hormone: a short review

“…Litter size increases milk demand, and this demand increases the secretion of prolactin, a hormone critical in the regulation of maternal care [ 23 ]. Rat mPOA MCH neurons express prolactin receptor mRNA [ 43 ], and prolactin pretreatment in both mice and rats results in the upregulation of the phosphorylated signal transducer and activator of transcription 5 (pSTAT5) transcription factor, a measure of prolactin receptor activation [ 43 ]. The consequences of prolactin on the MCH system appear complex, both the presence and absence of prolactin have been reported to attenuate transient MCH expression.…”

“…However, genetic knockout of the STAT5 gene, which inhibits prolactin receptor activation and functionally mimics blocking the effects of prolactin, also decreases MCH expression [ 92 ]. This reduction of transient MCH expression in the mPOA is also seen with the pharmacological reduction of circulating prolactin during lactation [ 43 ]. While these data implicate prolactin as a major factor regulating transient mPOA MCH neurons, further work will need to be undertaken to more precisely delineate the mechanistic effects of prolactin on transient mPOA MCH expression.…”