Estradiol Down-Regulates RF-Amide-Related Peptide (RFRP) Expression in the Mouse Hypothalamus
Open accessAbstract
In most mammals, RF-amide-related peptides are synthesized in the dorsomedial hypothalamic nucleus and regulate reproduction via inhibiting GnRH neurons and, possibly, adenohypophyseal gonadotrophs. In the present study, we investigated the possibility that RFRP-synthesizing neurons are involved in estrogen feedback signaling to the reproductive axis in mice. First, we used quantitative in situ hybridization and compared the expression of prepro-RFRP mRNA of ovariectomized mice, with and without 17β-estradiol (E2) replacement. Subcutaneous administration of E2 via silastic capsules for 4 d significantly down-regulated prepro-RFRP mRNA expression. The underlying receptor mechanism was investigated with immunohistochemistry. In ovariectomized mice, low levels of nuclear estrogen receptor (ER)-α immunoreactivity were detectable in 18.7 ± 3.8% of RFRP neurons. The majority of RFRP neurons showed no ER-α signal, and RFRP neurons did not exhibit ER-β immunoreactivity. Results of these studies indicate that RFRP is a negatively estradiol-regulated neurotransmitter/neuromodulator in mice. The estrogenic down-regulation of RFRP expression may contribute to estrogen feedback to the reproductive axis. The issue of whether E2 regulates RFRP neurons directly or indirectly remains open given that ER-α immunoreactivity is present only at low levels in a subset of these cells.
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E2 lowers RFRP-3 expression in mouse DMN, though only about 20% of RFRP-3 neurons have detectable ERα and none have ERβ.
“E2 reduces RFRP-3 expression in the DMN of mice, although only ~20% of RFRP-3 neurons express detectable levels of ERα protein and no detectable ERβ53.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [53]
Figure 1 (p. 4) shows that E2 reduced prepro-RFRP mRNA in the mouse dorsomedial nucleus. The receptor results (pp. 4–5) found detectable ERα in 18.7 ± 3.8% of RFRP neurons and no detectable ERβ. The paper measured precursor mRNA and identified neurons using RFRP-1 immunoreactivity; it did not specifically measure RFRP-3 expression or establish those receptor percentages for RFRP-3-identified neurons. (LLM, conf=0.86)
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- Authors
- Molnár, C. S., Kalló, I., Liposits, Z., & Hrabovszky, E.
- Affiliations
- Pázmány Péter Catholic University (HU)
- Corresponding author
- Hrabovszky, E.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2011-02-15
- Volume
- 152
- Issue
- 4
- Pages
- 1684-1690
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2039749586
- Cited by
- 80
- References
- 41
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 10 · 2015: 7 · 2014: 10 · 2013: 8 · 2012: 9
- FWCI
- 10.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- public-domain
- Locations
- Endocrinology (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Funders
- Takeda Pharmaceutical Company
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- estradiol, estrogen feedback, hypothalamus, dorsomedial hypothalamus, estrogen receptor alpha, estrogen receptor beta, ovariectomy, GnRH neurons, reproductive axis, estrogen regulation of gene expression
- MeSH terms
- Animals, Estradiol, Hypothalamus, Immunohistochemistry, Neuropeptides, RNA, Messenger, In Situ Hybridization, Estrogen Receptor alpha, Estrogen Receptor beta, Mice
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