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Search for other papers by L. G. CLEMENS in
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Search for other papers by B. A. GLADUE in
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Intracerebral infusion of prostaglandin E2 (PGE2) facilitated copulatory behaviour of longterm castrated rats. Castrated rats were given daily systemic injections of testosterone propionate (50 pg) or oil vehicle, and then 30 min before behavioural testing they received an intrahypothalamic infusion of either PGE2 or saline. Rats receiving PGE2 in addition to systemic testosterone showed more copulatory behaviour than those receiving PGE2 or testosterone alone.
Search for other papers by L. W. CHRISTENSEN in
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Search for other papers by L. G. CLEMENS in
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SUMMARY
Experiments were carried out to assess the possible involvement of cyclic AMP in the regulation of masculine sexual behaviour by testosterone in the laboratory rat. Doses of testosterone propionate which were ineffective in maintaining or inducing male sexual behaviour were potentiated by concurrent administration of theophylline. Since removal of the adrenal glands had no effect on this potentiation, the possibility that theophylline increased adrenal androgen secretion and thereby influenced sexual behaviour, can be ruled out. A major effect of theophylline is to increase levels of cyclic AMP by inhibiting the enzyme which inactivates this nucleotide. These results suggest that cyclic AMP may play a mediating role in the regulation of masculine sexual behaviour by testosterone.
Search for other papers by LINDA P. CONIGLIO in
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Search for other papers by D. C. PAUP in
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Search for other papers by L. G. CLEMENS in
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SUMMARY
Oestrogen—progesterone-induced lordosis behaviour was suppressed in female hamsters which received neonatal treatment with testosterone propionate or diethylstilboestrol. No suppression of lordosis was observed in females which received neonatal treatment with testosterone, androsterone or control substances. In addition, the ano—genital distance and diameter of the vaginal orifice were increased in females treated with testosterone, testosterone propionate, androsterone or diethylstilboestrol. However, testosterone, testosterone propionate and androsterone had a greater effect on ano—genital distance than did diethylstilboestrol. Possible mechanisms for the defeminizing action of the hormones administered were discussed.
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Search for other papers by G Rosiepen in
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Search for other papers by H Krishnamurthy in
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Search for other papers by M Arslan in
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Search for other papers by G Clemen in
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Search for other papers by GF Weinbauer in
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Although the gonadotropic control of the spermatogenic process is well established, the endocrine regulation of the timing and kinetics of germ cell development has received little attention. We found previously that the administration of a GnRH antagonist (ANT) over a period of 25 days could retard spermatid development and slightly prolong cycle length in intact adult cynomolgus monkeys (Macaca fascicularis). The aim of the present study was to investigate the effects of extended exposure to ANT on the duration of the cycle of the seminiferous epithelium in the monkey. Additionally, the duration of spermatogenesis was studied in the ANT-exposed rat model. In experiment 1, monkeys were given either saline or ANT (n=6/group) and on day 30 all animals received a single injection of 5-bromodeoxyuridine (BrdU) to label S-phase germ cells. Testicular biopsies were taken on days 39, 43, 47 and 51 (end of treatment) for BrdU localization and flow cytometric analysis. ANT treatment suppressed hormone levels, reduced testis size by >70% and severely impaired germ cell production. Despite these alterations, cycle duration remained unchanged at all time-points compared with controls (10.12+/-0.15 days vs 10.16+/- 0.44 days). In experiment 2, adult male Sprague-Dawley rats (n=15/group) received either vehicle (VEH) or ANT for 14 days and received BrdU injection on day 2. Cycle duration was found to be shorter in the ANT-treated group (12.45+/-0.09 days) than in the control group (12.75+/-0.08, P<0.05). As spermatogenic cycle length in this control group was longer than that of our historical controls (range: 12.37-12.53 days), experiment 2 was repeated (n=10/group). In experiment 3, cycle duration was 12.51+/-0.02 for VEH and 12.46+/-0.05 for the ANT-treated group (P>0.05) in both species. We concluded that the duration of the cycle of the seminiferous epithelium in monkeys and rats is independent of gonadotropins but is rather regulated by the spermatogenic tissue itself.
Search for other papers by Victoria E DeMambro in
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Search for other papers by Masanobu Kawai in
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Search for other papers by Thomas L Clemens in
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Search for other papers by Leah Rae Donahue in
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A spontaneous mouse mutant, designated ‘small’ (sml), was recognized by reduced body size suggesting a defect in the IGF1/GH axis. The mutation was mapped to the chromosome 1 region containing Irs1, a viable candidate gene whose sequence revealed a single nucleotide deletion resulting in a premature stop codon. Despite normal mRNA levels in mutant and control littermate livers, western blot analysis revealed no detectable protein in mutant liver lysates. When compared with the control littermates, Irs1 sml /Irs1 sml (Irs1 sml/sml ) mice were small, lean, hearing impaired; had 20% less serum IGF1; were hyperinsulinemic; and were mildly insulin resistant. Irs1 sml/sml mice had low bone mineral density, reduced trabecular and cortical thicknesses, and low bone formation rates, while osteoblast and osteoclast numbers were increased in the females but not different in the males compared with the Irs1 +/+ controls. In vitro, Irs1 sml/sml bone marrow stromal cell cultures showed decreased alkaline phosphatase-positive colony forming units (pre-osteoblasts; CFU-AP+) and normal numbers of tartrate-resistant acid phosphatase-positive osteoclasts. Irs1 sml/sml stromal cells treated with IGF1 exhibited a 50% decrease in AKT phosphorylation, indicative of defective downstream signaling. Similarities between engineered knockouts and the spontaneous mutation of Irs1 sml were identified as well as significant differences with respect to heterozygosity and gender. In sum, we have identified a spontaneous mutation in the Irs1 gene associated with a major skeletal phenotype. Changes in the heterozygous Irs1 + /sml mice raise the possibility that similar mutations in humans are associated with short stature or osteoporosis.
