Tac1-Ovulation SIGNED
Addressing the Roles of Tachykinins in the Control of Ovulation: Focus on the Substance-P/Tachykinin Receptor Type 1 (Tac1/Tacr1) System
Total Cost €
0EC-Contrib. €
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Project "Tac1-Ovulation" data sheet
The following table provides information about the project.
| Coordinator |
UNIVERSIDAD DE CORDOBA
Organization address contact info |
| Coordinator Country | Spain [ES] |
| Total cost | 172˙932 € |
| EC max contribution | 172˙932 € (100%) |
| Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
| Code Call | H2020-MSCA-IF-2019 |
| Funding Scheme | MSCA-IF-EF-RI |
| Starting year | 2020 |
| Duration (year-month-day) | from 2020-05-01 to 2022-04-30 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | UNIVERSIDAD DE CORDOBA | ES (CORDOBA) | coordinator | 172˙932.00 |
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Project objective
Reproductive health is deteriorating worldwide, via as yet unknown mechanisms. The most common cause of in/subfertility in women is ovulatory dysfunction; anovulation being associated to conditions as polycystic ovary syndrome, hypothalamic amenorrhea and premature ovarian insufficiency. Hence, better understanding of the mechanisms controlling ovulation is mandatory for improved management of reproductive disorders. While hypothalamic GnRH neurons are the major output pathway for the brain control of ovulation, upstream Kiss1 neurons, particularly in the rostral hypothalamic area in rodents, have been suggested to be crucial for the timed activation of GnRH neurons and generation of the preovulatory surge of gonadotropins that drives ovulation. However, the major regulators of this Kiss1/GnRH pathway remains ill defined. Substance P (SP, encoded by Tac1), a member of the tachykinin (TAC) family that acts via the receptor, NK1R (encoded by Tacr1), has been shown to centrally regulate gonadotropin release, and, according to our preliminary data, might modulate the pre-ovulatory surge in mice. Yet, the patho-physiological relevance of SP/NK1R signaling in ovulatory control needs to be defined. Here, we will apply functional genomics and virogenetic approaches to assess the roles and mechanisms of action of SP/NK1R signaling in the control of ovulation, with special attention to its actions in Kiss1 and GnRH neurons. To this end, we will apply (i) virogenetic-driven Tacr1 silencing in Kiss1 and GnRH neurons; (ii) tracing techniques to map Tac1 neuronal projections to Kiss1 and GnRH neurons; and (ii) chemo-genetic manipulation of Tac1 neurons, via excitatory and inhibitory DREADDs, coupled to monitoring of gonadotropin secretion and ovulation. Our project, which is based on our solid preliminary data, will expand our understanding of the mechanisms controlling ovulation and female fertility, helping to define novel strategies for reproductive control in the future.
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