ON TESTIS AND EPlDlDYMlS OF RATS - Pondicherry University ...

lmn~unization of monkeys against FSH either actively or passively has been shown to
be associated with disruption of fertility and a decline in sperm concentrations. It has
been reported that the specific spermatogonial subtypes are affected by withdrawal of
FSH alone (Moudgal et al., 1997). FSH has been shown to promote spermatogenesis
and fertility in primates (Moudgal and Sairam, 1998).
Administration of highly
purified FSH to GnRH antagonist treated monkeys has been shown to niaintnin
spermatogonial numbers (Weinbauer el a/., 1991). Actions of FSI-I on Sertoli cells
from prepubertal animals have been reported biochemically by increased estradiol
production (Fritz et al., 1976). It has been reported that FSH P-subunit gene knocked
out mice. rendering them FSH deficient showed that spermatogenesis could proceed
to completion albeit in the presence of smaller testes (Kumar et al., 1997). The
binding of LH to Leydig cells in the interstitial compartment of testis has been
reported to stimulate testosterone synthesis.
Initiation of spermatogenesis by testosterone and dehydrotestosterone has been
reported in mouse (Singh el al.. 1995).
Testosterone alone has been shown to
maintain spermatogenesis qualitatively in a dose-dependent fashion in monkeys
(Weinhnuer el (11.. 1988).
A high concentration of tcstosteronc within thc
seminiferous tubules LH has been shown to play a role in the initiation and
maintenance of sperm production in mouse (di Zerega and Sherins, 1980; Matsumota
and Bremmer. 1987).
In rodents and primates, by virtue of its local production.
intratesticular testosterone levels have been shown to be elevated approximately 100
fold above those in serum (Huhtaniemi er al., 1987).
A role for estrogens in normal spermatogenesis has also been reported (Hess ef
ul.. 1997) and at least two major steps have been shown to be influenced by estrogens
in the seminiferous tubules, stem cell number and spermatid maturation (Hess cr ul.,
1997). It has been shown that in virro multiplicntion of rat gonocytes is controlled by
growth factors and estradiol, which corresponds well with the presence of ERP in
these cells (Hess et a!., 2000).
In estrogen receptor a knockout (ERKOa) mouse
estrogens are necessary for the achievement of fertility (Hess et al.. 2000).