The Effects of Daily Administration of Single and Multiple Injections of Gonadotropin-Releasing Hormone on Pituitary and Gonadal Function in the Hypogonadal (hpg) Mouse*

Effect of eCG Administration on the Reproductive Function in Hypogonadal (hpg) Male Mice.

“…These results agreed with previous observations in hypophysectomized animals [14]. The duration for these processes and the composition of the germ cells in hpg mice were quite similar to those in normal mice [15], although the response to hormone therapy of the hpg mice was much weaker than that of hypophysectomized mice [5,16,17].…”

“…Many previous stuides [14,[18][19][20] have reported that eCG was effective for completing spermatogenesis, but single administration of GnRH did not induce whole spermatogenesis [5]. A daily injection of GnRH may have less stimulation to produce androgen, because weight of seminal vesicles after 60 days of GnRH administration in hpg mice was lower than that of mice given eCG for 60 days.…”

“…In the present study, a 1 µg/day/mouse dose of GnRH, seemed to be enough for inducing maturation of spermatozoa. This dose could induce ovulation in female rats, and it increased FSH and LH contents in male pituitary glands [5,21].…”

Estrogenic induction of spermatogenesis in the hypogonadal (hpg) mouse: role of androgens

“…The hpg mouse is an excellent animal model in which to investigate the mechanism of action of estrogens on spermatogenesis because it has arrested reproductive development without the need for surgical, endocrine, pharmacological or immunological intervention. This mouse line is infertile due to a congenital deficiency of hypothalamic gonadotropin-releasing hormone (GnRH) synthesis leading to markedly reduced pituitary contents of luteinizing hormone (LH) and FSH and undetectable or barely measurable serum gonadotropin levels (Cattanach et al 1977, Charlton et al 1983. Consequently, the testes fail to undergo normal postnatal development and, at an adult age, hpg testicular androgen production is barely detectable (Sheffield & O'Shaughnessy 1989, Scott et al 1990.…”

Le rôle du neuropeptide GnRH dans la cascade gonadotrope enfin validé dans l’espèce humaine

“…Le GNRH1, localisé chez l'homme sur le bras court du chromosome 8 en 8p21-p11.2, contient 4 exons séparés gnrh1 était transcrit mais aucune immunoréactivité de la GnRH n'était détectée dans l'hypothalamus. Ainsi, bien que les neurones à GnRH soient normalement présents et correctement localisés au niveau de l'hypothalamus, il n'y avait pas, chez les souris hpg, de sécrétion du décapeptide mature [7,8]. Le lien entre le génotype et le phénotype a été apporté par la réversion du phénotype grâce à l'introduction par transgenèse d'un fragment de 13,5 kb provenant du gène d'une souris normale [9].…”