<i>Kiss1</i>-dependent and independent release of luteinizing hormone and testosterone in perinatal male rats
-
- Chen Jing
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Minabe Shiori
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Munetomo Arisa
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Magata Fumie
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Sato Marimo
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Nakamura Sho
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
-
- Hirabayashi Masumi
- Center for Genetic Analysis of Behaviour, National Institute for Physiological Sciences, Aichi, Japan
-
- Ishihara Yasuhiro
- Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan
-
- Yamazaki Takeshi
- Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan
-
- Uenoyama Yoshihisa
- Graduate School of Bioagricultural Sciences, Nagoya University, Aichi, Japan
-
- Tsukamura Hiroko
- Graduate School of Bioagricultural Sciences, Nagoya University, Aichi, Japan
-
- Matsuda Fuko
- Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
Bibliographic Information
- Other Title
-
- Kiss1-Dependent and Independent Release of Luteinizing Hormone and Testosterone in Perinatal Male Rats
Search this article
Description
<p>Prenatal and postnatal biphasic increases in plasma testosterone levels derived from perinatal testes are considered critical for defeminizing/masculinizing the brain mechanism that regulates sexual behavior in male rats. Hypothalamic kisspeptin neurons are indispensable for stimulating GnRH and downstream gonadotropin, as well as the consequent testicular testosterone production/release in adult male rats. However, it is unclear whether kisspeptin is responsible for the increase in plasma testosterone levels in perinatal male rats. The present study aimed to investigate the role of Kiss1/kisspeptin in generating perinatal plasma LH and the consequent testosterone increase in male rats by comparing the plasma testosterone and LH profiles of wild-type (Kiss1+/+) and Kiss1 knockout (Kiss1–/–) male rats. A biphasic pattern of plasma testosterone levels, with peaks in the prenatal and postnatal periods, was found in both Kiss1+/+ and Kiss1–/– male rats. Postnatal plasma testosterone and LH levels were significantly lower in Kiss1–/– male rats than in Kiss1+/+ male rats, whereas the levels in the prenatal embryonic period were comparable between the genotypes. Exogenous kisspeptin challenge significantly increased plasma testosterone and LH levels and the number of c-Fos-immunoreactive GnRH neurons in neonatal Kiss1–/– and Kiss1+/+ male rats. Kiss1 and Gpr54 (kisspeptin receptor gene) were found in the testes of neonatal rats, but kisspeptin treatment failed to stimulate testosterone release in the cultured testes of both genotypes. These findings suggest that postnatal, but not prenatal, testosterone increase in male rats is mainly induced by central kisspeptin-dependent stimulation of GnRH and consequent LH release.</p>
Journal
-
- Endocrine Journal
-
Endocrine Journal 69 (7), 797-807, 2022
The Japan Endocrine Society