scholarly journals Reproductive neuroendocrinology of mammalian gonadotropin‐inhibitory hormone

2019 ◽  
Vol 18 (3) ◽  
pp. 225-233 ◽  
Author(s):  
Takayoshi Ubuka ◽  
Kazuyoshi Tsutsui
Keyword(s):  
Gonadotropin Inhibitory Hormone ◽  
Reproductive Neuroendocrinology

Normal Reproductive Neuroendocrinology in the Female

1993 ◽  
Vol 22 (1) ◽  
pp. 1-28 ◽  
Author(s):  
Stephen A. South ◽  
Vladimir I. Yankov ◽  
William S. Evans
Keyword(s):  
Reproductive Neuroendocrinology

scholarly journals Developmental changes in gonadotropin-inhibitory hormone in the Japanese quail (Coturnix japonica) hypothalamo-hypophysial system

2003 ◽  
Vol 178 (2) ◽  
pp. 311-318 ◽  
Author(s):  
T Ubuka ◽  
M Ueno ◽  
K Ukena ◽  
K Tsutsui
Keyword(s):  
Japanese Quail ◽  
Median Eminence ◽  
Anterior Pituitary ◽  
Coturnix Japonica ◽  
Developmental Changes ◽  
External Layer ◽  
Mature Peptide ◽  
Gonadotropin Release ◽  
Gonadotropin Inhibitory Hormone ◽  
Precursor Mrna

We previously isolated a novel dodecapeptide containing a C-terminal -Arg-Phe-NH(2) sequence, SIKPSAYLPLRF-NH(2) (RFamide peptide), from the Japanese quail (Coturnix japonica) brain. This novel quail peptide was shown to be located in neurons of the paraventricular nucleus (PVN) and their terminals in the median eminence (ME), and to decrease gonadotropin release from cultured anterior pituitary in adult birds. We therefore designated this peptide gonadotropin-inhibitory hormone (GnIH). Furthermore, a cDNA encoding the GnIH precursor polypeptide has been characterized. To understand the physiological roles of this peptide, in the present study we analyzed developmental changes in the expressions of GnIH precursor mRNA and the mature peptide GnIH during embryonic and posthatch ages in the quail diencephalon including the PVN and ME. GnIH precursor mRNA was expressed in the diencephalon on embryonic day 10 (E10) and showed a significant increase on E17, just before hatch. GnIH was also detected in the diencephalon on E10 and increased significantly around hatch. Subsequently, the diencephalic GnIH content decreased temporarily, and again increased progressively until adulthood. GnIH-like immunoreactive (GnIH-ir) neurons were localized in the PVN on E10, but GnIH-ir fibers did not extend to the ME. However, GnIH-ir neurons increased in the PVN on E17, just before hatch, and GnIH-ir fibers extended to the external layer of the ME, as in adulthood. These results suggest that GnIH begins its function around hatch and acts as a hypothalamic factor to regulate gonadotropin release in the bird.

scholarly journals Seasonally sympatric but allochronic: differential expression of hypothalamic genes in a songbird during gonadal development

2018 ◽  
Vol 285 (1889) ◽  
pp. 20181735 ◽  
Author(s):  
Carolyn M. Bauer ◽  
Adam M. Fudickar ◽  
Skylar Anderson-Buckingham ◽  
Mikus Abolins-Abols ◽  
Jonathan W. Atwell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Hormone Receptor ◽  
Gonadal Development ◽  
Luteinizing Hormone Receptor ◽  
Hpg Axis ◽  
Oestrogen Receptor Alpha ◽  
The Difference ◽  
Gonadal Recrudescence ◽  
Gonadotropin Inhibitory Hormone

Allochrony, the mismatch of reproductive schedules, is one mechanism that can mediate sympatric speciation and diversification. In songbirds, the transition into breeding condition and gonadal growth is regulated by the hypothalamic–pituitary–gonadal (HPG) axis at multiple levels. We investigated whether the difference in reproductive timing between two seasonally sympatric subspecies of dark-eyed juncos ( Junco hyemalis ) was related to gene expression along the HPG axis. During the sympatric pre-breeding stage, we measured hypothalamic and testicular mRNA expression of candidate genes via qPCR in captive male juncos. For hypothalamic mRNA, we found our earlier breeding subspecies had increased expression of gonadotropin-releasing hormone ( GnRH ) and decreased expression of androgen receptor, oestrogen receptor alpha and mineralocorticoid receptor ( MR ). Subspecies did not differ in expression of hypothalamic gonadotropin-inhibitory hormone ( GnIH ) and glucocorticoid receptor ( GR ). While our earlier breeding subspecies had higher mRNA expression of testicular GR , subspecies did not differ in testicular luteinizing hormone receptor, follicle-stimulating hormone receptor or MR mRNA expression levels. Our findings indicate increased GnRH production and decreased hypothalamic sensitivity to sex steroid negative feedback as factors promoting differences in the timing of gonadal recrudescence between recently diverged populations. Differential gene expression along the HPG axis may facilitate species diversification under seasonal sympatry.

scholarly journals Effects of Melatonin on Peripheral Reproductive Function: Regulation of Testicular GnIH and Testosterone

Endocrinology ◽  
2011 ◽  
Vol 152 (9) ◽  
pp. 3461-3470 ◽  
Author(s):  
Nicolette L. McGuire ◽  
Kristina Kangas ◽  
George E. Bentley
Keyword(s):  
Expression Patterns ◽  
Reproductive Function ◽  
Melatonin Receptors ◽  
Sex Steroid ◽  
European Starlings ◽  
Steroid Secretion ◽  
Local Inhibition ◽  
Gonadotropin Inhibitory Hormone ◽  
The Brain

Study of seasonal reproduction has focused on the brain. Here, we show that the inhibition of sex steroid secretion can be seasonally mediated at the level of the gonad. We investigate the direct effects of melatonin on sex steroid secretion and gonadal neuropeptide expression in European starlings (Sturnus vulgaris). PCR reveals starling gonads express mRNA for gonadotropin inhibitory hormone (GnIH) and its receptor (GnIHR) and melatonin receptors 1B (Mel 1B) and 1C (Mel 1C). We demonstrate that the gonadal GnIH system is regulated seasonally, possibly via a mechanism involving melatonin. GnIH/ GnIHR expression in the testes is relatively low during breeding compared with outside the breeding season. The expression patterns of Mel 1B and Mel 1C are correlated with this expression, and melatonin up-regulates the expression of GnIH mRNA in starling gonads before breeding. In vitro, GnIH and melatonin significantly decrease testosterone secretion from LH/FSH-stimulated testes before, but not during, breeding. Thus local inhibition of sex steroid secretion appears to be regulated seasonally at the level of the gonad, by a mechanism involving melatonin and the gonadal GnIH system.

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