دورية أكاديمية

Developmental GnRH signaling is not required for sexual differentiation of kisspeptin neurons but is needed for maximal Kiss1 gene expression in adult females.

التفاصيل البيبلوغرافية
العنوان: Developmental GnRH signaling is not required for sexual differentiation of kisspeptin neurons but is needed for maximal Kiss1 gene expression in adult females.
المؤلفون: Kim J; Department of Reproductive Medicine, University of California, San Diego, Leichtag Building 3A-15, 9500 Gilman Drive, No. 0674, LA Jolla, CA 92093, USA., Tolson KP, Dhamija S, Kauffman AS
المصدر: Endocrinology [Endocrinology] 2013 Sep; Vol. 154 (9), pp. 3273-83. Date of Electronic Publication: 2013 Jul 03.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: United States NLM ID: 0375040 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1945-7170 (Electronic) Linking ISSN: 00137227 NLM ISO Abbreviation: Endocrinology Subsets: MEDLINE
أسماء مطبوعة: Publication: 2017- : New York : Oxford University Press
Original Publication: Los Angeles, Calif. : Association for the Study of Internal Secretions,
مواضيع طبية MeSH: Sex Differentiation*/drug effects , Signal Transduction* , Up-Regulation*/drug effects, Gonadotropin-Releasing Hormone/*metabolism , Kisspeptins/*metabolism , Neurons/*metabolism , Thalamic Nuclei/*metabolism, Animals ; Anterior Thalamic Nuclei/cytology ; Anterior Thalamic Nuclei/drug effects ; Anterior Thalamic Nuclei/growth & development ; Anterior Thalamic Nuclei/metabolism ; Estradiol/pharmacology ; Estradiol/therapeutic use ; Estrogen Receptor alpha/chemistry ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Estrogen Replacement Therapy ; Estrogens/pharmacology ; Estrogens/therapeutic use ; Female ; Gonadotropin-Releasing Hormone/genetics ; Hypogonadism/drug therapy ; Hypogonadism/metabolism ; Hypogonadism/pathology ; Intralaminar Thalamic Nuclei/cytology ; Intralaminar Thalamic Nuclei/drug effects ; Intralaminar Thalamic Nuclei/growth & development ; Intralaminar Thalamic Nuclei/metabolism ; Kisspeptins/biosynthesis ; Kisspeptins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/agonists ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/cytology ; Neurons/drug effects ; Ovariectomy/adverse effects ; Sexual Development/drug effects ; Thalamic Nuclei/cytology ; Thalamic Nuclei/drug effects ; Thalamic Nuclei/growth & development
مستخلص: Kisspeptin, encoded by Kiss1, stimulates reproduction. In rodents, one Kiss1 population resides in the hypothalamic anterior ventral periventricular nucleus and neighboring rostral periventricular nucleus (AVPV/PeN). AVPV/PeN Kiss1 neurons are sexually dimorphic (greater in females), yet the mechanisms regulating their development and sexual differentiation remain poorly understood. Neonatal estradiol (E₂) normally defeminizes AVPV/PeN kisspeptin neurons, but emerging evidence suggests that developmental E₂ may also influence feminization of kisspeptin, although exactly when in development this process occurs is unknown. In addition, the obligatory role of GnRH signaling in governing sexual differentiation of Kiss1 or other sexually dimorphic traits remains untested. Here, we assessed whether AVPV/PeN Kiss1 expression is permanently impaired in adult hpg (no GnRH or E₂) or C57BL6 mice under different E₂ removal or replacement paradigms. We determined that 1) despite lacking GnRH signaling in development, marked sexual differentiation of Kiss1 still occurs in hpg mice; 2) adult hpg females, who lack lifetime GnRH and E₂ exposure, have reduced AVPV/PeN Kiss1 expression compared to wild-type females, even after chronic adulthood E₂ treatment; 3) E₂ exposure to hpg females during the pubertal period does not rescue their submaximal adult Kiss1 levels; and 4) in C57BL6 females, removal of ovarian E2 before the pubertal or juvenile periods does not impair feminization and maximal adult AVPV/PeN Kiss1 expression nor the ability to generate LH surges, indicating that puberty is not a critical period for Kiss1 development. Thus, sexual differentiation still occurs without GnRH, but GnRH or downstream E₂ signaling is needed sometime before juvenile development for complete feminization and maximal Kiss1 expression in adult females.
References: N Engl J Med. 2003 Oct 23;349(17):1614-27. (PMID: 14573733)
J Neurosci. 2008 Aug 27;28(35):8691-7. (PMID: 18753370)
Endocrinology. 2006 Dec;147(12):5817-25. (PMID: 16959837)
Biol Reprod. 2009 Dec;81(6):1216-25. (PMID: 19684332)
J Neurosci. 2005 Dec 7;25(49):11349-56. (PMID: 16339030)
Neuroendocrinology. 1990 Dec;52(6):581-8. (PMID: 2126608)
PLoS One. 2010 Jul 30;5(7):e11911. (PMID: 20689830)
Endocrinology. 2007 Apr;148(4):1774-83. (PMID: 17204549)
Endocrinology. 2012 Apr;153(4):1875-86. (PMID: 22374971)
J Reprod Dev. 2007 Apr;53(2):367-78. (PMID: 17213691)
Endocrinology. 2005 Sep;146(9):3686-92. (PMID: 15919741)
Proc Natl Acad Sci U S A. 2009 Oct 6;106(40):17217-22. (PMID: 19805188)
Endocrinology. 2012 Feb;153(2):782-93. (PMID: 22202164)
J Neurobiol. 1990 Jul;21(5):781-6. (PMID: 2394991)
Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10972-6. (PMID: 12944565)
Endocrinology. 2010 Dec;151(12):5807-17. (PMID: 20926580)
Nat Neurosci. 2008 Sep;11(9):995-7. (PMID: 19160494)
Front Neuroendocrinol. 2013 Jan;34(1):3-17. (PMID: 22728025)
J Comp Neurol. 2011 Oct 15;519(15):2954-77. (PMID: 21484804)
Brain Res Rev. 2008 Mar;57(2):277-87. (PMID: 17604108)
Biol Reprod. 2013 Jun 13;88(6):146. (PMID: 23595904)
Neurotoxicology. 2009 May;30(3):350-7. (PMID: 19442818)
Endocrinology. 2011 May;152(5):2020-30. (PMID: 21363930)
Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1761-6. (PMID: 15665093)
Endocrinology. 2011 Feb;152(2):595-606. (PMID: 21190958)
Horm Behav. 2004 Apr;45(4):242-9. (PMID: 15053940)
J Mol Neurosci. 2011 Feb;43(2):138-45. (PMID: 20665248)
Horm Behav. 2009 May;55(5):597-604. (PMID: 19446076)
Endocrinology. 2004 Sep;145(9):4073-7. (PMID: 15217982)
Horm Behav. 2010 Apr;57(4-5):390-5. (PMID: 19945459)
Endocrinology. 2009 Aug;150(8):3664-71. (PMID: 19443569)
Brain Res Dev Brain Res. 1990 Mar 1;52(1-2):17-23. (PMID: 2331785)
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15682-7. (PMID: 16230634)
Front Neuroendocrinol. 2005 Oct-Dec;26(3-4):163-74. (PMID: 16309736)
Endocrinology. 2009 Jul;150(7):3214-20. (PMID: 19299459)
J Neurosci. 2006 Jun 21;26(25):6687-94. (PMID: 16793876)
Endocrinology. 2008 May;149(5):2333-40. (PMID: 18202134)
معلومات مُعتمدة: U54-HD012303 United States HD NICHD NIH HHS; T32 HD007203 United States HD NICHD NIH HHS; U54 HD028934 United States HD NICHD NIH HHS; U54 HD-28934 United States HD NICHD NIH HHS; R01HD065856 United States HD NICHD NIH HHS; P50 HD012303 United States HD NICHD NIH HHS; U54 HD012303 United States HD NICHD NIH HHS; P50 HD028934 United States HD NICHD NIH HHS; R01 HD065856 United States HD NICHD NIH HHS
المشرفين على المادة: 0 (Estrogen Receptor alpha)
0 (Estrogens)
0 (Kiss1 protein, mouse)
0 (Kisspeptins)
0 (Nerve Tissue Proteins)
33515-09-2 (Gonadotropin-Releasing Hormone)
4TI98Z838E (Estradiol)
تواريخ الأحداث: Date Created: 20130705 Date Completed: 20131112 Latest Revision: 20220309
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC3749477
DOI: 10.1210/en.2013-1271
PMID: 23825121
قاعدة البيانات: MEDLINE
الوصف
تدمد:1945-7170
DOI:10.1210/en.2013-1271