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Addressing the Roles of Tachykinins in the Control of Ovulation: Focus on the Substance-P/Tachykinin Receptor Type 1 (Tac1/Tacr1) System

Project description

A better understanding of ovulation to improve female fertility

Ovulatory dysfunction is a common cause of women's infertility, often associated with conditions such as polycystic ovary syndrome, hypothalamic amenorrhea or premature ovarian insufficiency. Hypothalamic gonadotropin-releasing hormone-expressing (GnRH) neurons control the release of reproductive hormones from the pituitary gland. It has been suggested that upstream Kiss1 neurons are crucial for the activation of GnRH neurons and the preovulatory surge of gonadotropins leading to ovulation. Substance P, a member of the neuron tachykinin neuropeptide family, has been shown to regulate gonadotropin release and might modulate the preovulatory surge in mice. The EU-funded Tac1-Ovulation project will apply functional genomics to assess the role of substance P signalling in Kiss1 and GnRH neurons in the process of ovulation.

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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MSCA-IF-EF-RI - RI – Reintegration panel

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(opens in new window) H2020-MSCA-IF-2019

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Coordinator

UNIVERSIDAD DE CORDOBA
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 172 932,48
Address
AVENIDA DE MEDINA AZAHARA 5
14005 CORDOBA
Spain

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Region
Sur Andalucía Córdoba
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 172 932,48
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