Interactions of gonadotropin-releasing hormone (GnRH) and gonadotropin-inhibitory hormone (GnIH) in birds and mammals

2006 ◽  
Vol 305A (9) ◽  
pp. 807-814 ◽  
Author(s):  
George E. Bentley ◽  
Lance J. Kriegsfeld ◽  
Tomohiro Osugi ◽  
Kazuyoshi Ukena ◽  
Sara O'brien ◽  
...  
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gonadotropin Inhibitory Hormone

Neuroanatomical Organization of the Brain Gonadotropin-Inhibitory Hormone and Gonadotropin-Releasing Hormone Systems in the Frog Pelophylax esculentus

2014 ◽  
Vol 85 (1) ◽  
pp. 15-28 ◽  
Author(s):  
Claudia Pinelli ◽  
Arun G. Jadhao ◽  
Saikat P. Biswas ◽  
Kazuyoshi Tsutsui ◽  
Biagio D''Aniello
Keyword(s):  
Preoptic Area ◽  
Anterior Commissure ◽  
Medial Septum ◽  
Gonadotropin Releasing Hormone ◽  
Gonadotropin Secretion ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Medial Septal Area ◽  
Gonadotropin Inhibitory Hormone ◽  
The Brain

Growing evidence suggests that gonadotropin-inhibitory hormone (GnIH) may play a key role in mediating vertebrate reproduction. GnIH inhibits gonadotropin synthesis and release by decreasing the activity of gonadotropin-releasing hormone (GnRH) neurons as well as by directly regulating gonadotropin secretion from the pituitary. Whereas the presence of GnIH has been widely investigated in various classes of vertebrates, there are very few immunohistochemical reports focusing on GnIH in amphibians. The aim of this study was to assess the presence and neuroanatomical distribution of GnIH-like immunoreactivity in the brain of the anuran amphibian Pelophylax (Rana) esculentus (esculenta) and to explore any potential anatomical relationship with mammalian GnRH-immunoreactive (mGnRH-ir) elements. The GnIH-like immunoreactive (GnIH-ir) system constitutes two distinct subpopulations in the telencephalon and diencephalon, with the highest number of immunoreactive cells located in the preoptic and suprachiasmatic areas. GnIH-ir neurons were also observed in the medial septum, the anterior commissure, the dorsal hypothalamus, the periventricular nucleus of the hypothalamus, and the posterior tuberculum. Scattered GnIH-ir fibers were present in all major subdivisions of the brain but only occasionally in the median eminence. mGnRH-ir neurons were distributed in the mediobasal telencephalon, the medial septal area, and the anterior preoptic area. Double-label immunohistochemistry revealed that the GnRH and GnIH systems coexist and have overlapping distributions at the level of the anterior preoptic area. Some GnIH-ir fibers were in close proximity to mGnRH-ir cell bodies. Our results suggest that both the neuroanatomy and the functional regulation of GnRH release are conserved properties of the hypothalamic GnIH-ir system among vertebrate species.

Role of RFRP-3 in the Regulation of Kiss-1 Gene Expression in the AVPV Hypothalamic Cell Model mHypoA-50

2018 ◽  
Vol 26 (9) ◽  
pp. 1249-1255 ◽  
Author(s):  
Haruhiko Kanasaki ◽  
Tuvshintugs Tumurbaatar ◽  
Aki Oride ◽  
Zolzaya Tumurgan ◽  
Hiroe Okada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Positive Feedback ◽  
Messenger Rna ◽  
Cell Model ◽  
Reproductive Function ◽  
Feedback Regulation ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gonadotropin Inhibitory Hormone

Kisspeptin, encoded by the Kiss-1 gene, plays a crucial role in reproductive function by governing the hypothalamic–pituitary–gonadal axis. The recently established Kiss-1-expressing cell model mHypoA-50 displays characteristics of neuronal cells of the anteroventral periventricular (AVPV) region of the mouse hypothalamus. Because Kiss-1 gene expression in these cells is upregulated by estradiol (E2), mHypoA-50 cells are regarded as a valuable model for the study of Kiss-1-expressing neurons in the AVPV region. These cells also express RFamide-related peptide-3 (RFRP-3), a mammalian homolog of gonadotropin inhibitory hormone. The RFRP-3 expression in mHypoA-50 cells was increased by melatonin stimulation. In addition, E2 stimulation increased RFRP-3 expression in these cells. Treatment of the mHypoA-50 cells with exogenous RFRP-3 resulted in the increase of Kiss-1 messenger RNA expression within the cells; however, RFRP-3 did not modify gonadotropin-releasing hormone or kisspeptin-induced Kiss-1 gene expression in these cells. In addition, we found that RFRP-3 stimulation increased the expression of corticotropin-releasing hormone, which may be involved in E2-induced positive feedback in mHypoA-50 cells. Our observations suggest that RFRP-3 might be involved in positive feedback regulation by directly or indirectly increasing Kiss-1 gene expression.

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