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Department of Veterinary Preclinical Sciences, University of Glasgow Veterinary School (P.J.O., P.B.), Glasgow, Scotland G61 1QH; the Department of Human Anatomy, University of Oxford (U.S., H.M.C.), Oxford, United Kingdom OX1 3QX; and the Department of Physiology, University of Turku (A.-M.H., I.H.), 20520 Turku, Finland
Address all correspondence and requests for reprints to: Prof. P. J. O’Shaughnessy, Department of Veterinary Preclinical Sciences, University of Glasgow Vet School, Bearsden Road, Glasgow, Scotland G61 1QH. E-mail: P.J.OShaughnessy{at}vet.gla.ac.uk
During fetal development the testes secrete anti-Mullerian hormone and
testosterone to induce formation of the male phenotype. Adult Leydig
cells secrete testosterone under the control of LH, but the role of the
fetal pituitary in regulating fetal Leydig cell function is unclear. To
study the early relationship between pituitary and Leydig cell
function, we have examined the development of fetal pituitary LH levels
and Leydig cell function in normal mice and in hypogonadal
(hpg) mice that lack GnRH and, thus, circulating
gonadotropins. In normal and hpg mice, pituitary LH
content was barely detectable until embryonic day 17 (E17), when levels
began to increase significantly in both groups. Pituitary levels of LH
in hpg mice were, however, only about 10% of normal at
all ages. Full-length LH receptor transcripts were first detectable in
fetal testes on E16 in both normal and hpg mice. In
normal mice, levels of testicular messenger RNA (mRNA) encoding
cytochrome P450 side-chain cleavage and 17
-hydroxylase increased
from E13 to reach a peak around birth. In hpg mice,
levels of mRNA encoding these enzymes were normal until around birth,
at which time there was a significant decline. Levels of testicular
mRNA encoding 3ß-hydroxysteroid dehydrogenase type I were similar in
normal and hpg mice and showed little change during
development. Intratesticular testosterone reached a peak on E18 in
normal animals before declining again after birth. In
hpg mice, intratesticular testosterone levels were
normal throughout fetal development and on the day of birth, but were
barely detectable by postnatal day 5. Results show 1) that fetal Leydig
cell function in the mouse is normal in the absence of endogenous
circulating gonadotropins; 2) that Leydig cells become dependent on
gonadotropins shortly after birth; and 3) that pituitary LH synthesis
can start in the absence of GnRH but is dependent on LH for a normal
level of synthesis and secretion
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