Cited by 145Hypothalamic control of reproductive hormonesGrowth Hormone and Insulin-like Growth FactorsNeuroendocrine regulation and behavior

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Prolactin Regulation of Gonadotropin-Releasing Hormone Neurons to Suppress Luteinizing Hormone Secretion in Mice

Grattan, David R., Jasoni, Christine L., Liu, Xinhuai, Anderson, Greg M., Herbison, Allan E.·2007·Endocrinology

DOI 10.1210/en.2007-0403

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Abstract

Hyperprolactinemia causes infertility, but the mechanisms involved are not known. The present study aimed to determine whether and how prolactin may influence LH secretion in the adult female mouse. Using ovariectomized, estrogen-treated (OVX+E) mice, we found that 7 d of intracerebroventricular prolactin potently suppressed serum LH levels (P < 0.05). To examine whether this central action of prolactin may involve the GnRH neurons, the effects of acute and chronic prolactin on cAMP response element-binding protein phosphorylation (pCREB) in GnRH neurons were examined using dual-label immunocytochemistry. In diestrous and OVX+E mice, a single sc injection of ovine prolactin resulted in a significant (P < 0.05) doubling of the number of GnRH neurons expressing pCREB. OVX+E mice treated with five injections of ovine prolactin over 48 h showed a 4-fold increase in the number of GnRH neurons with pCREB. To determine whether GnRH neurons might be regulated directly by prolactin, we examined prolactin receptor (PRL-R) mRNA expression in green fluorescent protein-tagged GnRH neurons by single-cell RT-PCR. As a positive control, PRL-R mRNA was measured in arcuate dopaminergic neurons obtained from green fluorescent protein-tagged tyrosine hydroxylase neurons. Three of 23 GnRH neurons (13%) were identified to express PRL-R transcripts, whereas nine of 11 arcuate dopaminergic neurons (82%) were found to coexpress PRL-R mRNA. These data demonstrate that prolactin suppresses LH levels in the mouse, as it does in other species, and indicate that it acts centrally to regulate intracellular signaling within GnRH neurons. This is likely to occur, at least in part, through the direct regulation of a subpopulation of GnRH neurons.

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Authors: Grattan, D. R., Jasoni, C. L., Liu, X., Anderson, G. M., & Herbison, A. E.
Affiliations: University of Otago (NZ)
Corresponding author: Grattan, David R.
ORCID: Grattan, David R.
Jasoni, Christine L.
Liu, Xinhuai
Anderson, Greg M.
Herbison, Allan E.
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2007-09-01
Volume: 148
Issue: 9
Pages: 4344-4351
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2007-0403
OpenAlex: W2109374960
Cited by: 145
References: 69
Citations by year: 2026: 1 · 2025: 7 · 2024: 11 · 2023: 5 · 2022: 8 · 2021: 9 · 2020: 4 · 2019: 10 · 2018: 10 · 2017: 8 · 2016: 9 · 2015: 6 · 2014: 9 · 2013: 5 · 2012: 10
FWCI: 10.31
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: Wellcome Trust
Topics: Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
Keywords: prolactin, luteinizing hormone secretion, GnRH neurons, hyperprolactinemia, prolactin receptor, CREB phosphorylation, cAMP signaling, female fertility
MeSH terms: Animals, Cerebral Ventricles, Estrus, Homeostasis, Injections, Intraventricular, Luteinizing Hormone, Gonadotropin-Releasing Hormone, Male, Mice, Inbred C57BL, Neurons, Ovariectomy, Phosphorylation, Prolactin, Cyclic AMP Response Element-Binding Protein, Mice

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Prolactin Regulation of Gonadotropin-Releasing Hormone Neurons to Suppress Luteinizing Hormone Secretion in Mice

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