Abstract
The newly described hypothalamic peptide, phoenixin, is produced in the hypothalamus and adenohypophysis, where it acts to control reproductive hormone secretion. Both phoenixin and its receptor GPR173 are expressed in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, suggesting additional, nonreproductive effects of the peptide to control vasopressin (AVP) or oxytocin (OT) secretion. Hypothalamo-neurohypophysial explants released AVP but not OT in response to phoenixin. Intracerebroventricular administration of phoenixin into conscious, unrestrained male and female rats significantly increased circulating AVP, but not OT, levels in plasma, and it increased immediate early gene expression in the supraoptic nuclei of male rats. Bath application of phoenixin in hypothalamic slice preparations resulted in depolarization of PVN neurons, indicating a direct, neural action of phoenixin in the hypothalamus. Our results suggest that the newly described, hypothalamic peptide phoenixin, in addition to its effects on hypothalamic and pituitary mechanisms controlling reproduction, may contribute to the physiological mechanisms regulating fluid and electrolyte homeostasis.
Recommended Citation
S. Gasparini et al., "Novel Regulator of Vasopressin Secretion: Phoenixin," American Journal of Physiology Regulatory Integrative and Comparative Physiology, vol. 314, no. 4, pp. R623 - R628, American Physiological Society, Apr 2018.
The definitive version is available at https://doi.org/10.1152/ajpregu.00426.2017
Department(s)
Biological Sciences
Publication Status
Open Access
Keywords and Phrases
Electrophysiology; Hypothalamus; Oxytocin; Phoenixin; Radioimmuno-assay; Vasopressin
International Standard Serial Number (ISSN)
1522-1490; 0363-6119
Document Type
Article - Journal
Document Version
Final Version
File Type
text
Language(s)
English
Rights
© 2025 American Physiological Society, All rights reserved.
Creative Commons Licensing

This work is licensed under a Creative Commons Attribution 4.0 License.
Publication Date
16 Apr 2018
PubMed ID
29364701

Comments
National Institutes of Health, Grant HL-121456