PUBLICATION

Paracrine/autocrine control of spermatogenesis by gonadotropin-inhibitory hormone

Authors
Fallah, H.P., Tovo-Neto, A., Yeung, E.C., Nóbrega, R.H., Habibi, H.R.
ID
ZDB-PUB-190507-13
Date
2019
Source
Molecular and Cellular Endocrinology   492: 110440 (Journal)
Registered Authors
Keywords
Flutamide (FLU), Gonadotropin-inhibitory hormone (gnih), Human chorionic gonadotropin (hCG), Spermatids (SPD), Spermatozoa (SPZ), Testosterone, Zebrafish gnih (zGnih)
MeSH Terms
  • Animals
  • Autocrine Communication*/drug effects
  • Gene Expression Regulation, Developmental/drug effects
  • Gonadotropins/pharmacology
  • Leydig Cells/metabolism
  • Male
  • Neuropeptides/genetics*
  • Neuropeptides/metabolism
  • Paracrine Communication*/drug effects
  • Spermatids/growth & development
  • Spermatids/metabolism
  • Spermatogenesis*/drug effects
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed
31048005 Full text @ Mol. Cell. Endocrinol.
Abstract
Control of testicular development is multifactorial and involves a number of hypothalamic, hypophyseal and peripheral hormones. Here, we investigated direct action of zebrafish gonadotropin-inhibitory hormone (zGnih) which is expressed in the testis, on spermatogenesis in zebrafish, in vitro. Treatment with zGnih at the lower doses (10 and 100 nM) inhibited gonadotropin-induced spermatids/spermatozoa (SPD/SPZ) production. However, at the highest dose (1000 nM), zGnih increased basal number of SPD/SPZ and showed paradoxical effect. The effects of zGnih on testosterone and SPD/SPZ production was blocked in the presence of androgen receptor antagonist, flutamide (FLU). A number of transcripts were also measured to better understand zGnih mechanisms of action on zebrafish spermatogenesis. Our results provide strong support for the hypothesis that locally produced zGnih is a component of the complex multifactorial system that regulates testicular development and function in adult zebrafish, in part, by changes in testicular steroidogenesis and regulation of gonadotropin-induced response.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping