PUBLICATION

Integrated Role of Arginine Vasotocin in the Control of Spermatogenesis in Zebrafish

Authors
Zanardini, M., Habibi, H.R.
ID
ZDB-PUB-251230-13
Date
2025
Source
International Journal of Molecular Sciences   26: (Journal)
Registered Authors
Keywords
AVT, arginine vasotocin, in vivo, paracrine hormonal regulation, reproductive physiology, spermatogenesis
MeSH Terms
  • Animals
  • Cell Proliferation/drug effects
  • Follicle Stimulating Hormone/pharmacology
  • Male
  • Receptors, FSH/genetics
  • Receptors, FSH/metabolism
  • Spermatogenesis*/drug effects
  • Spermatogonia/cytology
  • Spermatogonia/drug effects
  • Spermatogonia/metabolism
  • Spermatozoa/drug effects
  • Spermatozoa/metabolism
  • Testis/drug effects
  • Testis/metabolism
  • Testosterone/analogs & derivatives
  • Testosterone/blood
  • Vasotocin*/metabolism
  • Vasotocin*/pharmacology
  • Zebrafish*/metabolism
  • Zebrafish*/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
41465365 Full text @ Int. J. Mol. Sci.
Abstract
Arginine vasotocin (AVT) has recently emerged as a local regulator of testicular function in fish. Using ex vivo culture system, it was demonstrated that AVT directly stimulates androgen-dependent basal spermatogenesis in zebrafish. In the presence of gonadotropins, AVT enhanced FSH-induced development of early phases of spermatogonial proliferation while blocking FSH-mediated spermiogenesis. However, AVT promoted proliferation of LH-induced pre-meiotic and meiotic germ cell populations without affecting the final stages of spermiogenesis. These findings led to the hypothesis that AVT plays a role by promoting early germ cell proliferation and differentiation while simultaneously inhibiting premature progression through spermiogenesis. To test this hypothesis, we investigated the chronic effects of AVT on adult zebrafish testes, in vivo. Prolonged AVT treatment for 21 days led to dose-dependent accumulation of undifferentiated type A spermatogonia and reduced post-meiotic germ cells and spermatozoa. We also observed decreased plasma 11-ketotestosterone (11-KT) levels and downregulation of fshr. This was accompanied by a basal suppression of avt and its receptors, avpr1aa, avpr1ab, avpr2aa, avpr2ab, avpr2l, in both brain and testis during the pre-spawning phase. The present findings, along with those of previously published studies, collectively demonstrate that AVT presence during the early stages of testicular development promotes spermatogonia proliferation while diminishing FSH-induced premature progress toward spermatogenesis. This occurs until later stages, when AVT expression is diminished, allowing for optimal LH-induced spermiogenesis in zebrafish.
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