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Biomedical subjects

W H Moger

Publications and source records attributed to W H Moger.

At least 37 records · Page 2Linked to original sources
PubMed1984

Periventricular and suprachiasmatic lesion effects on photoperiodic responses of the hamster hypophyseal-gonadal axis.

We examined the involvement of neural mechanisms within the suprachiasmatic nucleus (SCN) and periventricular area (PVA), and the role of prolactin (Prl) in control of endocrine function in short day-exposed Syrian hamsters. Hamsters bearing lesions of the SCN or PVA, hamsters implanted with an anterior pituitary under the kidney capsule to provide sustained Prl levels, and sham-operated hamsters were exposed to either 14L:10D or 8L:16D. After 9 wk, hamsters were sacrificed, and their testes and pituitaries were studied in vitro to assess their secretory capacity. SCN lesions and large periventricular lesions impinging on the paraventricular nucleus prevented testicular regression during short-day exposure. Small periventricular lesions and pituitary implants did not prevent gonadal regression in hamsters exposed to short days. Testis weights were positively correlated with basal and luteinizing hormone (LH)-stimulated androgen production in the control and lesioned groups; pituitary implants prevented the decline in androgen production in vitro in gonadally regressed animals. The relative in vitro pituitary response to gonadotropin-releasing hormone (GnRH) stimulation in control and lesioned groups was not reduced by short-day exposure. These data indicate that either axons coursing dorsally from the SCN or extra-SCN structures in the periventricular/paraventricular area are necessary for testicular regression in short photoperiods.

Androgens↗
PubMed1984

Ontogeny of rodent testicular androgen production in response to isoproterenol and luteinizing hormone in vitro.

The ontogeny of rodent testicular androgen production in response to the catecholamine agonist L-isoproterenol (Isop) and luteinizing hormone (LH) was studied in vitro. Isop (10(-4) M) significantly increased rat androgen production by 1.2- 3.3-fold on Days 18.5 to 21.5 of gestation and on Days 1 to 60 of postnatal life during the 3-h incubation in Medium 199. Similarly, Isop augmented mouse androgen production by 1.4- to 4.3-fold on Days 16.5 to 19.5 of gestation and on 1, 10, 20 40 and 60 days of postnatal life. No effect of the beta-agonist was observed in postnatal rats aged 6 and 10 days, and mice aged 2, 5, 15 and 30 days. In both species, LH (100 ng/ml) induced large increases (2.8- to 265.6-fold) in androgen production at all fetal and postnatal ages. Isop was 0.3-22.9% as effective as LH in the two species. The minimum concentration of Isop to significantly increase androgen production by testes from 20.5-day rat fetuses was 10(-8) M, while 10(-5) M was required to stimulate 17.5-day mouse fetuses. Isop significantly increased androgen production by 20.5-day rat and 17.5-day mouse fetuses after a time lag of 30 and 180 min, respectively. In both species, a beta-adrenergic antagonist, propranolol (10(-5) M), abolished the increased androgen production attributed to Isop. Propranolol alone and the D-isomer of Isop had no effect. The results indicate that although LH is the key stimulant of testicular androgen production, catecholamines may play an important role(s) in testicular development, especially at fetal ages.

Adrenergic beta-Agonists↗
PubMed1984

Constant lighting conditions affect sexual behaviour and hormone levels in adult male rats.

Adult male Long-Evans rats (90 days of age) were housed in 12 h light: 12 h dark (Group LD), constant white light (Group LL), or constant dark (dim red light) (Group DD) for 60-90 days. The first of two sexual behaviour tests revealed that more (P less than 0.05) rats in Group LD achieved intromission than did those in Groups LL and DD. Only 33% of Group LL and 32% of Group DD rats ejaculated. In contrast, all Group LD rats that mounted eventually ejaculated. Males in Group LD achieved more (P less than 0.05) ejaculations (mean of both tests combined, 3.4) than did males in Groups LL (1.5) or DD (1.2). Although there were no notable differences amongst the groups in the weights of the accessory sex organs, males in Group DD had higher (P less than 0.05) serum androgen levels than did those in Groups LL and LD while Group LL males had higher (P less than 0.05) serum prolactin levels than did those in Groups LD and DD. There were no differences in LH or FSH levels. In addition, more rats in Group LL had disrupted activity rhythms than did Group DD rats. These results indicate that housing in constant white or dim red light disrupts sexual behaviour in male rats and may do so through different neuroendocrine mechanisms.

Androgens↗
PubMed1983

Hormonal correlates of parental behavior in male rats.

Groups of seven intact male Long-Evans hooded rats were housed with pups for 1, 7, 14, or 22 days and their parental behavior was recorded each day. All but one male showed parental behavior. Twenty-eight control males were housed without pups. At the end of each observation period the males were decapitated and their trunk blood was collected for hormone analysis by radioimmunoassay. Males with pups had lower prolactin levels than control males on all 4 days but did not differ in luteinizing hormone, follicle-stimulating hormone, or testosterone levels from males without pups. Both prolactin and testosterone levels were correlated positively with the frequency of parental behavior, suggesting that the males which are behaviorally the most responsive to infants are also hormonally the most responsive.

Animals↗
PubMed1983

Neural regulation of the ovary: evidence for hypothalamic asymmetry in endocrine control.

The effects of hypothalamic hemi-islands on ovarian compensatory hypertrophy (OCH) were determined in prepubertal female rats. In animals with hypothalamic hemi-islands on the left side, OCH was blocked in rats hemi-ovariectomized on the ipsi- but not the contralateral side. A potential asymmetrical involvement of the hypothalamus in OCH was suggested by the further observation that this phenomenon could not be demonstrated in rats given hypothalamic hemi-islands on the right side and hemi-ovariectomized on the ipsi- or contralateral side. These data suggest that in addition to a possible direct neural contribution to endocrine feedback, the two-halves of the hypothalamus may differ in terms of their sensitivity to various components of endocrine control.

Animals↗
PubMed1983

Effects of the calcium-channel blockers cobalt, verapamil, and D600 on Leydig cell steroidogenesis.

The effects of various calcium-channel blockers on androgen production by collagenase-dispersed mouse testicular interstitial cells were investigated. Cobalt caused a dose-dependent inhibition of the maximum rate of luteinizing hormone (LH)-stimulated androgen production without altering the concentration of LH required for half maximum stimulation (EC50). Nickel and manganese also inhibited LH-stimulated steroidogenesis but were less potent than cobalt. The major site at which cobalt treatment inhibited steroidogenesis was beyond cAMP formation and before 3 beta-hydroxysteroid dehydrogenase. This conclusion was based on the observation that cobalt inhibited dibutyryl cAMP-stimulated androgen production but did not affect protein synthesis and pregnenolone-supported androgen production. Androgen production was unaffected by the organic calcium-channel blockers verapamil and the (+) and (-) enantiomers of D600 at concentrations less than 0.1 mM. At a concentration of 0.1 mM the organic calcium-channel blockers inhibited LH- and dibutyryl cAMP-stimulated androgen production. Unlike cobalt, the organic calcium-channel blockers also inhibited pregnenolone-supported androgen production and reduced the rate of protein synthesis. Similarities between the effects of cobalt in the present study and previous reports of the effects of reduced extracellular calcium concentrations on androgen production suggest that cobalt inhibits androgen production as a result of its ability to block calcium influx. The calcium channels involved in the steroidogenic process appear, however, to be relatively insensitive to the organic calcium-channel blockers.

Androgens↗
PubMed1983

Photoperiodic modification of opiate but not beta-adrenergic or benzodiazepine binding sites in hamster brain.

Exposure to short photoperiods induces gonadal regression in the golden hamster. This is accompanied by a fall in serum gonadotropins and changes in hypothalamic neurotransmitter turnover. We have attempted to correlate these changes with alterations in neurotransmitter receptor binding parameters. Compared to hamsters held in long photoperiods, opiate ([3H] naloxone) binding in hamsters exposed to short photoperiods is elevated in whole brain and in cerebral cortex but not in hypothalamus. However, beta-adrenergic ([3H] dihydroalprenolol) and benzodiazepine ([3H] flunitrazepam) binding are unaffected in whole brain, cerebral cortex or hypothalamus. Thus, changes in hypothalamic noradrenaline turnover rate previously reported may not be correlated with changes in beta-adrenergic binding.

Alprenolol↗
PubMed1983

Effects of forskolin on androgen production by mouse interstitial cells in vitro. Interactions with luteinizing hormone and isoproterenol.

Micromolar concentrations of the diterpene forskolin stimulated androgen production by collagenase-dispersed mouse testicular interstitial cells. With maximum stimulatory concentrations, forskolin and luteinizing hormone (LH) increased androgen production with similar time courses and to similar extents. The concentration of LH required for half-maximum stimulation (EC50) was reduced approximately 10-fold in the presence of forskolin whereas maximum androgen production was unaffected. Likewise, LH reduced the EC50 for forskolin approximately 5-fold. The observed synergism between LH and forskolin was most likely at the level of cAMP generation as forskolin did not alter the EC50 for dibutyryl cAMP activation of androgen production. When cells were allowed to attach to the wells of tissue culture plates for 3 h prior to stimulation, isoproterenol treatment induced a small increase in androgen production when, and only when, submaximum concentrations of forskolin were also present. The increase in androgen production attributable to isoproterenol was blocked by simultaneous exposure to the beta-antagonist propranolol. When cells were immediately (O h) exposed to forskolin and isoproterenol, no interaction was observed. These results demonstrate the ability of forskolin treatment to reveal the presence of "latent" beta-adrenergic receptors. They also indicate that isolated adult mouse Leydig cells may not contain such receptors.

Androgens↗
PubMed1983

beta-adrenergic agonist induced androgen production during primary culture of mouse Leydig cells.

Mouse testicular interstitial cells and Leydig cells prepared by density-gradient centrifugation developed the ability to increase androgen production in response to isoproterenol between 24 and 48 hr of primary culture. Although exposure of the cultures to isoproterenol or cycloheximide inhibited the acquisition of responsiveness to beta-adrenergic stimulation, in vivo treatment with propranolol did not alter the time at which cultures became responsive to isoproterenol. It is concluded that the acquisition of beta-agonist responsiveness during culture is not a recovery from beta-adrenergic desensitization.

Adrenergic beta-Agonists↗
PubMed1982

Ipsilateral hypothalamic deafferentation blocks the increase in serum FSH following hemi-castration.

In two experiments hypothalamic hemi-islands or sham surgeries were produced on the right side of prepubertal male rats with an extrudable Halàsz-type knife (1.5 mm radius). Animals were then sham castrated or else hemi-castrated on the contralateral or ipsilateral side with respect to brain surgery. Eight or 21 days later, hemi-castrated rats given sham knife cuts showed a significant increase in serum FSH, relative to sham animals with intact testes. Also, animals given hypothalamic hemi-islands and hemi-castrated on the contralateral side showed a significant increase in serum FSH comparable to that seen in hemi-castrated rats with sham brain surgeries. However, hypothalamic hemi-island rats which were hemi-castrated on the ipsilateral side failed to show an increase in serum FSH and were similar to sham operated controls with both gonads. Serum LH levels were comparable among all groups, verifying a clear dissociation between LH and FSH secretion associated with hemi-castration in prepubertal males. In addition, the differences between contralateral and ipsilateral hemi-castrated animals with identical unilateral brain surgeries strongly suggest that FSH release is, in part, under direct neural control. However, in a third experiment, differences in FSH release between ipsi- and contralateral hemi-castrated rats were not found in animals with hypothalamic hemi-islands on the left side of the brain. Thus the hypothalamus may be asymmetrically involved in various components of neuroendocrine control.

Afferent Pathways↗
PubMed1982

Reevaluation of the effect of follicle-stimulating hormone on the steroidogenic capacity of the testis: the effects of neuraminidase-treated FSH preparations.

The ability of FSH treatment to increase the amount of androgen produced by the testis in response to maximum LH stimulation may be an effect of the LH contamination of the FSH preparations. To examine this question, 3 FSH preparations of different potencies and degrees of LH contamination or their neuraminidase-treated derivatives were administered to hypophysectomized immature rats for 5 days. The capacity of the testes to produce androgens in vitro was assessed at the end of the treatment period. Neuraminidase treatment reduces the in vivo activity of ovine and bovine FSH but does not alter the activity of ovine or bovine LH. Neuraminidase treatment of one FSH preparation (NH-bFSH-B1) did not reduce the ability of this FSH preparation to increase the response of the testis to LH stimulation in vitro. This suggests that the considerable LH contamination of the NIH-bFSH-B1 may be responsible for its effect. However, neuraminidase treatment of 2 more highly purified FSH preparations (bFSH-199C and NIH-oFSH-S13) abolished or greatly reduced the ability of these preparations to increase testicular weight and the response to LH in vitro. It is concluded that the ability of highly-purified FSH preparations to increase the amount of androgen produced by the testis is due to FSH activity and not the contaminating LH.

Androgens↗
PubMed1982

Short-term primary culture of mouse interstitial cells: effects of culture conditions of androgen production.

This study examined the effects of culture conditions and hormone treatment on androgen production by mouse interstitial cells in short-term primary culture. Testicular interstitial cells (18-25% 3 beta-hydroxysteriod dehydrogenase-positive) were maintained in serum-free hormone supplemented medium. Basal (nonstimulated) androgen production was found to be plating-density dependent. Androgen production per cell increased dramatically in a time- and cell concentration-dependent manner. This effect was reproduced in low density cultures by addition of charcoal-stripped conditioned medium from high density cultures. The cell anchorage factors, fibronectin and poly-l-lysine, similarly enhanced basal androgen production but did not augment responsiveness to luteinizing hormone (LH). Coating of the culture surface with serum inhibited androgen production. Cultured cells remained responsive to LH for 4 to 5 days and both insulin (5 micrograms/ml) and epidermal growth factor (EGF) (3 ng/ml) augmented LH-stimulated androgen production. There was a transient increase in LH sensitivity and maximum LH-stimulated androgen production for 5 to 72 h in culture followed by a decline in androgen production to low levels after 4 to 5 days in culture. This loss of activity was partially prevented by addition of antioxidants to the medium or by reduction of the ambient O2 concentration to 1%.

Androgens↗
PubMed1982

Monodansylcadaverine inhibition of testicular 17-ketosteroid reductase.

Dispersed mouse testicular interstitial cells were treated with the transglutaminase inhibitor monodansylcadaverine (500 microM) for 30 min. Subsequent incubation of the cells with [3H]pregnenolone increased formation of steroidogenic intermediates, tentatively identified as progesterone, 17 alpha-hydroxyprogesterone, and androstenedione, but decreased testosterone formation by monodansylcadaverine-treated cells. Measurement of 17-ketosteroid reductase activity (the enzyme that converts androstenedione to testosterone) demonstrated that monodansylcadaverine treatment caused a reversible, noncompetitive inhibition of this enzyme. These results suggest that transglutaminase catalyzed protein cross-links may influence the activity of 17-ketosteroid reductase.

17-Hydroxysteroid Dehydrogenases↗
PubMed1981

Circadian surges of LH in the ovariectomised rat occur coincident with enhanced pituitary responsiveness to GnRH.

Experiments are described in which we have investigated the responsiveness to GnRH of pituitary glands obtained from ovariectomised rats in which LH surges were induced by steroid priming (a) by estrogen implants and (b) by estrogen-progesterone injections. These treatments generate LH surges late in the light phase. Stimulation with GnRH in vitro revealed a large increase in responsiveness coincident with the surge of LH. We suggest that this effect is mediated through a self-priming effect of GnRH and that this in vitro technique may be used to detect hypothalamic release of GnRH.

Animals↗
PubMed1981

Transpubertal modulation of pituitary and testicular function in the ob/ob mouse.

We have investigated developmental, transpubertal, changes in the responsiveness to stimulation of pituitary gland and testes from the male ob/ob mouse. These organs were removed from ob/ob mice at 33 and 90 days after birth and stimulated with GnRH and LH, respectively, in vitro. Pituitary glands from lean mice released significantly more LH than those from ob/ob mice at both ages. In contrast, FSH release was higher in young ob/ob mice but not significantly different at 90 days when compared with lean controls. LH-stimulated testes revealed that although the young ob/ob testes released significantly less testosterone (T) than lean controls, the response became normal after the time of expected puberty. The production of 5 alpha-androstane-3 alpha, 17 beta-diol (DIOL), although reduced at both ages in ob/ob mice, declined transpubertally in both lean and ob/ob mice. As a result, the ratio of T:DIOL which normally becomes much greater than 1 with the advent of puberty, also increases to greater than 1 in the ob/ob males, suggesting that sexual maturation of testicular androgen biosynthesis is approximately normal. We conclude that the differences in pituitary and testicular response to stimulation could arise from a defect in the ability of the pituitary gland to release gonadotrophins.

Androstane-3,17-diol↗
PubMed1981

Development of a quotidian increase in pituitary responsiveness to GnRH in prepubertal female rats.

Pituitaries from immature male and female rats (5, 13, 21, 27 and 30 days of age) were removed at 08:00 or 16:00 h and stimulated with GnRH in vitro. In female rats more LH was released from pituitaries taken at 16:00 h than at 08:00 h on Days 21, 27 and 30, but not on Days 5 and 13. There were no differences in male rats in responsiveness of pituitaries taken at these two times. The ability of GnRH to induce release of more LH in the late afternoon may help to synchronize hormone output to coincide with first ovulation.

Animals↗