Prolactin receptor in regulation of neuronal excitability and channels

Patil, Mayur; Henry, Michael; Akopian, Armen N.

doi:10.4161/chan.28946

Cited by 68 publications

(75 citation statements)

References 90 publications

(156 reference statements)

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“…This proposal is consistent with early evidence suggesting that dopamine turnover in the median eminence is reduced following acute stress . As outlined in the Introduction, prolactin receptor stimulation results in the activation of a number of intracellular signalling pathways, in addition to STAT5 phosphorylation, including those that result in excitation of TIDA neurones . The mechanism responsible for a reduced level of pSTAT5 in the TIDA neurones following stress is unknown.…”

Section: Discussionsupporting

confidence: 86%

“…Deletion studies have demonstrated that, in the mouse, neuronal prolactin signalling is exclusively mediated by STAT5b rather than STAT5a . However, it is important to note that, in addition to the STAT5 pathway, which is primarily directed at the regulation of gene expression, prolactin receptor activation can act via alternative mechanisms to rapidly change neuronal excitability …”

Section: Introductionmentioning

confidence: 99%

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Restraint stress increases prolactin‐mediated phosphorylation of signal transducer and activator of transcription 5 in the hypothalamus and adrenal cortex in the male mouse

Kirk

Xie

Steyn

et al. 2017

J Neuroendocrinology

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Prolactin is a pleiotropic peptide hormone produced by the lactotrophs in the anterior pituitary. Its rate of secretion is primarily regulated by a negative-feedback mechanism where prolactin stimulates the activity of the tuberoinfundibular dopaminergic (TIDA) neurones, increasing their release of dopamine, which accesses the pituitary via the median eminence to suppress further prolactin secretion. In addition to its well established role in lactation, circulating prolactin is secreted in response to stress, although the mechanism by which this is achieved or its cellular targets remains unknown. In the present study, we show that 15 minutes of restraint stress causes an approximately seven-fold increase in circulating prolactin concentration in male mice. Monitoring prolactin receptor activation, using immunohistochemistry to determine the level and distribution of tyrosine phosphorylated signal transducer and activator of transcription 5 (pSTAT5), we show that this stress-induced increase in prolactin interacts with both central and peripheral targets. Restraint stress for 15 minutes significantly increased pSTAT5 staining in the arcuate nucleus, median eminence and the zona fasciculata of the adrenal cortex. In each case, this response was prevented by pretreating the animals with bromocriptine to block prolactin secretion from the pituitary. Interestingly, in contrast to many cells in the arcuate nucleus, stress reduced pSTAT5 staining of the TIDA neurones (identified by dual-labelling for tyrosine hydroxylase). This suggests that there is reduced prolactin signalling in these cells and thus potentially a decline in their inhibitory influence on prolactin secretion. These results provide evidence that prolactin secreted in response to acute stress is sufficient to activate prolactin receptors in selected target tissues known to be involved in the physiological adaptation to stress.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Restraint stress increases prolactin‐mediated phosphorylation of signal transducer and activator of transcription 5 in the hypothalamus and adrenal cortex in the male mouse

Kirk

Xie

Steyn

et al. 2017

J Neuroendocrinology

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“…Prolactin is known to stimulate lactation and mammary gland development, as well as facilitate milk production and secretion (Kennett and McKee, 2012;Patil et al, 2014). It has been proposed that the relationship between the capacity to dissipate heat and lactation is mediated by prolactin (Speakman and Król, 2005).…”

Section: Prolactin and Neuropeptide Gene Expression In The Hypothalamusmentioning

confidence: 99%

Sustained energy intake in lactating Swiss mice: a dual modulation process

Wen

Tan

Qiao

et al. 2017

Journal of Experimental Biology

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Limits to sustained energy intake (SusEI) during lactation are important because they provide an upper boundary below which females must trade off competing physiological activities. To date, SusEI is thought to be limited either by the capacity of the mammary glands to produce milk (the peripheral limitation hypothesis) or by a female's ability to dissipate body heat (the heat dissipation hypothesis). In the present study, we examined the effects of litter size and ambient temperature on a set of physiological, behavioral and morphological indicators of SusEI and reproductive performance in lactating Swiss mice. Our results indicate that energy input, energy output and mammary gland mass increased with litter size, whereas pup body mass and survival rate decreased. The body temperature increased significantly, while food intake (18 g day −1 at 21°C versus 10 g day −1 at 30°C), thermal conductance (lower by 20-27% at 30°C than 21°C), litter mass and milk energy output decreased significantly in the females raising a large litter size at 30°C compared with those at 21°C. Furthermore, an interaction between ambient temperature and litter size affected females' energy budget, imposing strong constraints on SusEI. Together, our data suggest that the limitation may be caused by both mammary glands and heat dissipation, i.e. peripheral limitation is dominant at room temperature, but heat dissipation is more significant at warm temperatures. Further, the level of the heat dissipation limits may be temperature dependent, shifting down with increasing temperature.

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“…Other functions of PRL also have been discovered. Patil et al report that PRL influences neuronal functions via activation of certain neurons, resulting in Ca(2+) influx and/or electrical firing with subsequent release of neurotransmitters [21]. It is suggested that PRL serves a critical role in breast cancer progression via activation of its cognate receptor [22].…”

Section: Discussionmentioning

confidence: 99%

Psychological Stress-Derived Prolactin Modulates Occludin Expression in Vaginal Epithelial Cells to Compromise Barrier Function

Liu

Song

2015

Cell Physiol Biochem

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This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Key Words Epithelial barrier • Psychological stress • Prolactin • Biological transport • T84 cellsAbstract Background/Aims: The causative factors of the vaginitis are not fully understood yet. Epithelial barrier dysfunction plays a critical role in the pathogenesis of vaginitis. This study aims to investigate the role of prolactin (PRL) in the causing the vaginal epithelial barrier dysfunction. Methods: Adult rats were treated with water-avoid-stress. The serum levels of PRL were determined by ELISA. T84 cell (T84 cells; a vaginal epithelial cell line) monolayers were prepared to be used assessing the epithelial barrier functions. The expression of occludin in T84 cells was assessed by Chromatin immunoprecipitation assay, methylation specific PCR, real time quantitative RT-PCR and Western blotting. Results: The results showed that psychological stress markedly increased the serum levels of PRL in the rat vaginal epithelia. Exposure of T84 cells to PRL in the culture markedly increased the phosphorylation of STAT3 and suppressed the expression of occludin in the cells; the transepithelial electric resistance was decreased and the permeability to a macromolecular tracer was increased in the T84 monolayers, which was mimicked by blocking STAT3, or abolished by over expression of occludin in the epithelial cells. Conclusions: Psychological stress-derived PRL induces vaginal epithelial barrier dysfunction by inhibiting the expression of occludin.

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Prolactin receptor in regulation of neuronal excitability and channels

Cited by 68 publications

References 90 publications

Restraint stress increases prolactin‐mediated phosphorylation of signal transducer and activator of transcription 5 in the hypothalamus and adrenal cortex in the male mouse

Restraint stress increases prolactin‐mediated phosphorylation of signal transducer and activator of transcription 5 in the hypothalamus and adrenal cortex in the male mouse

Sustained energy intake in lactating Swiss mice: a dual modulation process

Psychological Stress-Derived Prolactin Modulates Occludin Expression in Vaginal Epithelial Cells to Compromise Barrier Function

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