In vivo blockade of acetylcholinesterase increases intraovarian acetylcholine and enhances follicular development and fertility in the rat
Author
dc.contributor.author
Urra, Javier
Author
dc.contributor.author
Blohberger, Jan
Author
dc.contributor.author
Tiszavari, Michelle
Author
dc.contributor.author
Mayerhofer, Artur
Author
dc.contributor.author
Lara Peñaloza, Hernán
Admission date
dc.date.accessioned
2016-12-19T15:34:33Z
Available date
dc.date.available
2016-12-19T15:34:33Z
Publication date
dc.date.issued
2016
Cita de ítem
dc.identifier.citation
Scientific Reports Volumen: 6 Número de artículo: 3012 Jul 2016
es_ES
Identifier
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10.1038/srep30129
Identifier
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https://repositorio.uchile.cl/handle/2250/141956
Abstract
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Growth and differentiation of ovarian follicles are regulated by systemic and local factors, which may include acetylcholine (ACh). Granulosa cells (GCs) of growing follicles and luteal cells produce ACh and in cultured GCs it exerts trophic actions via muscarinic receptors. However, such actions were not studied in vivo. After having established that rat ovarian GCs and luteal cells express the ACh-metabolizing enzyme ACh esterase (AChE), we examined the consequences of local application of an AChE inhibitor, huperzine A (HupA), by osmotic minipump delivery into the ovarian bursa of hemiovariectomized rats. Saline was used in the control group. Local delivery of HupA for 4 weeks increased ovarian ACh content. Estrus cyclicity was not changed indicating a locally restricted range of HupA action. The number of primordial and primary follicles was unaffected, but small secondary follicles significantly increased in the HupA group. Furthermore, a significant increase in the number of corpora lutea suggested increased ovulatory events. In support, as shown upon mating, HupA-treated females had significantly increased implantation sites and more pups. Thus the data are in support of a trophic role of ACh in follicular development and ovulation and point to an important role of ACh in female fertility.
es_ES
Patrocinador
dc.description.sponsorship
Fondecyt grant
1130049
Deutsche Forschungsgemeinschaft (DFG)
MA 1080/19-1
MA 1080/19-2
Conicyt-PIA-DFG10 binational program