Canna~Fangled Abstracts

Spatial distribution of cannabinoid receptor 1 and fatty acid amide hydrolase in the cat ovary and oviduct.

By May 4, 2017No Comments
Acta Histochem. 2017 May 4. pii: S0065-1281(16)30334-8. doi: 10.1016/j.acthis.2017.04.007.
[Epub ahead of print]

Abstract

pm-2-site-207Involvement of the endocannabinoid system in female reproduction has been extensively described in humans with the cognate receptors and ligands being found in the ovaries and genital tract. In human, an imbalance of the endocannabinoid system is linked with both ectopic pregnancy and infertility. In bovine species anandamide levels regulate aspects of sperm-oviduct interaction. Here we report the immunohistochemical distribution of cannabinoid receptor 1 (CB1R) and fatty acid amide hydrolase (FAAH) in cat ovary and oviduct, using paraffin-embedded tissue samples and commercially available antibodies. We found a differential expression of both CB1R and FAAH during different stages of ovarian function and in the oviduct. CB1R was detected only in tertiary follicle granulosa cells while more immature follicles were negative. FAAH was instead found in ovarian pre-antral follicles, the oocyte cytoplasm, and in granulosa cells of primary, secondary and tertiary follicles. Secondary and tertiary follicles were also FAAH immunoreactive. Luteal cells were immunopositive for both CB1R and FAAH. Because CBR1 in oviduct was found only in ciliated cells, it might represent a specific marker at least in cats. In contrast, FAAH immunoreactivity was observed in both ciliated and non-ciliated cells. The present study may thus serve as the starting point for further investigations on the role of the endocannabinoid system in cat reproduction. Additional work will be needed to assess whether the morphological distribution of CB1R and FAAH changes in different conditions such as pre-pubertal age, follicular phase of the sexual cycle and pregnancy.

KEYWORDS:

CB1R; Cat; Endocannabinoid system; FAAH; Ovary; Oviduct

PMID: 28478955

 

DOI: 10.1016/j.acthis.2017.04.007
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