Document Detail


Localization of gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin and GnRH receptor and their possible roles in testicular activities from birth to senescence in mice.
MedLine Citation:
PMID:  23027641     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The changes in distribution and concentration of neuropeptides, gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin, and gonadotropin-releasing hormone receptor (GnRH-R) were evaluated and compared with reproductive parameters, such as cytochrome P450 side-chain cleavage (P450 SCC) enzyme activity, androgen receptors (AR) in the testis and serum testosterone levels, from birth to senescence in mice. The results showed the localization of these molecules mainly in the interstitial and germ cells as well as showed significant variations in immunostatining from birth to senescence. It was found that increased staining of testicular GnRH-R coincided with increased steroidogenic activity during pubertal and adult stages, whereas decreased staining coincides with decreased steroidogenic activity during senescence. Similar changes in immunostaining were confirmed by Western/slot blot analysis. Thus, these results suggest a putative role of GnRH during testicular pubertal development and senescence. Treatment with a GnRH agonist ([DTrp(6), Pro(9)-NEt] GnRH) to mice from prepubertal to pubertal period showed a significant increase in steroidogenic activity of the mouse testis and provided further support to the role of GnRH in testicular pubertal maturation. The significant decline in GnRH-R during senescence may be due to a significant increase in GnIH synthesis during senescence causing the decrease in GnRH-R expression. It is considered that significant changes in the levels of GnRH-R may be responsible for changes in steroidogenesis that causes either pubertal activation or senescence in testis of mice. Furthermore, changes in the levels of GnRH-R may be modulated by interactions among GnRH, GnIH, and kisspeptin in the testis.
Authors:
Shabana Anjum; Amitabh Krishna; Rajagopala Sridaran; Kazuyoshi Tsutsui
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-10-01
Journal Detail:
Title:  Journal of experimental zoology. Part A, Ecological genetics and physiology     Volume:  317     ISSN:  1932-5231     ISO Abbreviation:  J Exp Zool A Ecol Genet Physiol     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-19     Completed Date:  2013-04-18     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  101297745     Medline TA:  J Exp Zool A Ecol Genet Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  630-44     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
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MeSH Terms
Descriptor/Qualifier:
Aging / physiology*
Animals
Gene Expression Regulation / physiology
Glycoproteins / genetics,  metabolism*
Gonadotropin-Releasing Hormone / genetics,  metabolism*
Kisspeptins / genetics,  metabolism*
Male
Mice
Receptors, LHRH / genetics,  metabolism*
Testis / physiology*
Grant Support
ID/Acronym/Agency:
G12 RR003034/RR/NCRR NIH HHS; HD41749/HD/NICHD NIH HHS; HD52155/HD/NICHD NIH HHS; RR03034/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Glycoproteins; 0/Kisspeptins; 0/Receptors, LHRH; 0/gonadotropin inhibitor; 33515-09-2/Gonadotropin-Releasing Hormone
Comments/Corrections

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