Male juvenile spermatogonial depletion (jsd/jsd) mice are sterile because o
f a failure of spermatogonial differentiation. We have previously reported
the recovery of spermatogonial differentiation by suppressing the levels of
gonadotropins and testosterone with Nal-Glu, a GnRH antagonist. To determi
ne whether suppression of testosterone or the gonadotropins was responsible
for spermatogenic recovery, we examined the effect of supplementation of L
H or FSH along with Nal-Glu treatment. Systemic administration of flutamide
, an androgen receptor antagonist, was also examined. LH supplementation el
evated both serum and intratesticular testosterone levels and suppressed th
e recovery of spermatogonial differentiation in a dose-dependent manner. Su
pplementation with FSH did not affect either testosterone levels or spermat
ogonial differentiation. Furthermore, the mice treated with flutamide showe
d some recovery of spermatogonial differentiation. The overall findings rev
ealed that testosterone action mediated by androgen receptors suppressed th
e spermatogonial differentiation in jsd/jsd mice and suggested that spermat
ogonial differentiation in the jsd mutant is highly sensitive to testostero
ne suppression.