A Novel Mechanism Controlling Neurohypophyseal Hormone Release

• Grant number: 17/22140-0
• Support Opportunities: Scholarships abroad - Research Internship - Post-doctor
• Start date: February 01, 2018
• End date: January 31, 2019
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: José Antunes Rodrigues
• Grantee: Gislaine de Almeida Pereira
• Supervisor: Willis Kendrick Samson
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Institution abroad: Saint Louis University (SLU), United States
• Associated to the scholarship: 14/25005-8 - Interaction of cellular mechanisms of estradiol and Angiotensin II in the central structures involved in the control of body fluids: in vitro study, BP.PD

Abstract

A novel reproductive peptide was recently described and named Phoenixin (PHXN). The novel neuropeptide PHXN, discovered in 2013 by Yosten et al., and its receptor, GPR173, were identified in magnocellular neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON) suggesting a functional importance of PHXN on the control of the hydromineral homeostasis and a modulation on the hypothalamo-neurohypophysial system. In fact, previous studies from Yosten and Samson group showed that PHXN induces a significant vasopressin (AVP) but not oxytocin (OT) release in hypothalamo-neurohypophyseal explants and in conscious, unrestrained male rats. However, the mechanisms involved in AVP release induced by PHXN are unknown. Therefore, this study aims to investigate new mechanisms by which PHNX controls neurohypohyseal hormone release in response osmotic or hypovolemic stimuli. The elucidation of PHXN mechanisms related to neurohypophyseal release can provide important insights of its role in the modulation of hydromineral homeostasis, enhancing the knowledge of non-reproductive PHXN actions under physiological and pathophysiological conditions such as dehydration and hypovolemia.