GPER1 in sand rat epididymis: Effects of seasonal variations, castration and efferent ducts ligation.

Estrogen plays a crucial role in regulating epididymal function and development. Estrogen signaling is mediated via two main receptors essentially involved in the genomic regulating pathway: ERα and ERβ. Recent studies revealed the contribution of a novel estrogen receptor involved in the non-genomic pathway: GPER1. This receptor belongs to the family of seven-transmembrane G-protein-coupled receptors and it triggers rapid cellular responses. Immuno-histochemical studies and Western Blot analyses were performed to investigate the GPER1 expression in the caput and cauda epididymis of free-ranging fat sand rats (Psammomys obesus) captured during the breeding and resting seasons. We also investigated the effect of castration (C), castration followed by testosterone treatment (C+T), and ligation of the efferent ducts (L). During the breeding season, a marked positive GPER1 immunoreactivity was detected in the cytoplasm of principal cells and basal cells; this signal persisted during the resting season, attenuated however, meanwhile the clear cells were not immuno-reactive. In C animals, the immuno-histochemical staining underwent nuclear translocation. In C+T animals, this response became nuclear and cytoplasmic. In the L group, the expression of the GPER1 was mainly located in the cytoplasm of principal cells and in the nuclei of basal cells; the sperm was also immune-positive in the cauda epididymis. Western blot analysis showed that GPER1 has a molecular weight of 55kDa in the caput and cauda epididymis during the breeding season, and it persisted during the resting season in the caput epididymis with a decrease in the cauda epididymis. These results suggest that GPER1 mediate a specific cellular estrogen signaling with marked differences between the breeding and resting seasons. Experimental groups suggest that testosterone is involved in the regulation of the expression of GPER1, in addition to other estrogen signalization pathways.