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Publication : Prolactin receptor expression in mouse dorsal root ganglia neuronal subtypes is sex-dependent.

First Author  Patil M Year  2019
Journal  J Neuroendocrinol Volume  31
Issue  8 Pages  e12759
PubMed ID  31231869 Mgi Jnum  J:285629
Mgi Id  MGI:6392418 Doi  10.1111/jne.12759
Citation  Patil M, et al. (2019) Prolactin receptor expression in mouse dorsal root ganglia neuronal subtypes is sex-dependent. J Neuroendocrinol 31(8):e12759
abstractText  Sensory neurones exhibit sex-dependent responsiveness to prolactin (PRL). This could contribute to sexual dimorphism in pathological pain conditions. The present study aimed to determine the mechanisms underlying sex-dependent PRL sensitivity in sensory neurones. A quantitative reverse transcriptase-polymerase chain reaction shows that prolactin receptor (Prlr) long and short isoform mRNAs are expressed at comparable levels in female and male mouse dorsal root ganglia (DRG). In Prlr(cre/+) ;Rosa26(LSL-tDTomato/+) reporter mice, percentages of Prlr(+) sensory neurones in female and male DRG are also similar. Characterisation of Prlr(+) DRG neurones using immunohistochemistry and electrophysiology revealed that Prlr(+) DRG neurones are mainly peptidergic nociceptors in females and males. However, sensory neurone type-dependent expression of Prlr is sex dimorphic. Thus, Prlr(+) populations fell into three small- and two medium-large-sized sensory neuronal groups. Prlr(+) DRG neurones are predominantly medium-large sized in males and are proportionally more comprised of small-sized sensory neurones in females. Specifically, Prlr(+) /IB4(+) /CGRP(+) neurones are four- to five-fold higher in numbers in female DRG. By contrast, Prlr(+) /IB4(-) /CGRP(+) /5HT3a(+) /NPYR2(-) are predominant in male DRG. Prlr(+) /IB4(-) /CGRP(-) , Prlr(+) /IB4(-) /CGRP(+) and Prlr(+) /IB4(-) /CGRP(+) /NPYR2(+) neurones are evenly encountered in female and male DRG. These differences were confirmed using an independently generated single-cell sequencing dataset. Overall, we propose a novel mechanism by which sensory neurone type-dependent expression of Prlr could explain the unique sex dimorphism in responsiveness of nociceptors to PRL.
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