Document Detail


Opposite-sex housing reactivates the declining GnRH system in aged transgenic male mice with FGF signaling deficiency.
MedLine Citation:
PMID:  23047985     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The continued presence of gonadotropin-releasing hormone (GnRH) neurons is required for a healthy reproductive lifespan, but factors that maintain postnatal GnRH neurons have not been identified. To begin to understand these factors, we investigated whether 1) fibroblast growth factor (FGF) signaling and 2) interactions with the opposite sex are involved in the maintenance of the postnatal GnRH system. A transgenic mouse model (dnFGFR mouse) with the targeted expression of a dominant-negative FGF receptor (dnFGFR) in GnRH neurons was used to examine the consequence of FGF signaling deficiency on postnatal GnRH neurons. Male dnFGFR mice suffered a significant loss of postnatal GnRH neurons within the first 100 days of life. Interestingly, this loss was reversed after cohabitation with female, but not male, mice for 300-550 days. Along with a rescue in GnRH neuron numbers, opposite-sex housing in dnFGFR males also increased hypothalamic GnRH peptide levels, promoted a more mature GnRH neuronal morphology, facilitated litter production, and enhanced testicular morphology. Last, mice hypomorphic for FGFR3 exhibited a similar pattern of postnatal GnRH neuronal loss as dnFGFR males, suggesting FGF signaling acts, in part, through FGFR3 to enhance the maintenance of the postnatal GnRH system. In summary, we have shown that FGF signaling is required for the continued presence of postnatal GnRH neurons. However, this requirement is not absolute, since sexual interactions can compensate for defects in FGFR signaling, thereby rescuing the declining GnRH system. This suggests the postnatal GnRH system is highly plastic and capable of responding to environmental stimuli throughout adult life.
Authors:
Johanna R Rochester; Wilson C J Chung; Tyrone B Hayes; Pei-San Tsai
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-09
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-17     Completed Date:  2013-02-25     Revised Date:  2013-12-18    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1428-39     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Aging*
Animals
Cell Count
Fibroblast Growth Factor 3 / metabolism*
Gonadotropin-Releasing Hormone / metabolism*
Heterozygote
Hypothalamus / cytology,  growth & development,  metabolism*
Male
Mice
Mice, Knockout
Mice, Transgenic
Nerve Degeneration / etiology,  prevention & control
Nerve Tissue Proteins / genetics,  metabolism
Neurons / cytology,  metabolism*
Receptor, Fibroblast Growth Factor, Type 3 / genetics,  metabolism*
Receptors, LHRH / metabolism
Sexual Behavior, Animal
Signal Transduction*
Synaptic Transmission
Testis / cytology,  growth & development,  metabolism
Grant Support
ID/Acronym/Agency:
1F32AG-037257/AG/NIA NIH HHS; 5R01HD-04263/HD/NICHD NIH HHS; R00 HD058044/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Fgf3 protein, mouse; 0/Fibroblast Growth Factor 3; 0/Nerve Tissue Proteins; 0/Receptors, LHRH; 33515-09-2/Gonadotropin-Releasing Hormone; EC 2.7.10.1/Fgfr3 protein, mouse; EC 2.7.10.1/Receptor, Fibroblast Growth Factor, Type 3
Comments/Corrections

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