Nitric oxide control of steroidogenesis: endocrine effects of NG-nitro-L-arginine and comparisons to alcohol.

Recent studies suggest that nitric oxide (NO) may regulate hormone biosynthesis and secretion. This was tested by treating male rats with NG-nitro-L-arginine methyl ester (NAME), a NO synthase inhibitor, and measuring serum and testicular interstitial fluid testosterone and serum corticosterone, luteinizing hormone (LH), and prolactin (PRL). The effect of NG-nitro-L-arginine (NA), a less-soluble form of the same NO synthase inhibitor, on the reproductive suppressant actions of alcohol was also examined. NAME increased testosterone and corticosterone secretion dose-dependently without affecting LH and PRL secretion. The alcohol-induced suppression of testosterone or LH secretion was not altered by treatment with NA. Although effects of NAME and NA on other systems may be involved, these results indicate that testicular and adrenal steroidogenesis are negatively regulated by endogenous NO and that NO does not regulate LH and PRL secretion or inhibit the testicular steroidogenic pathway in the same way as alcohol.     

Pituitary and gonadal function during physical exercise in the male rat

The effects of training and acute exercise on serum testosterone, luteinizing hormone (LH) and corticosterone levels and on testicular endocrine function in male rats were studied. In the first part of the study, the rats were trained progressively on a treadmill, over 8 weeks. Training did not change the basal levels of serum testosterone, LH and corticosterone, or the testicular concentrations of testosterone and its precursors progesterone and androstenedione. The levels of testicular LH (30.3 +/- 2.6 ng/g wet wt, mean +/- SEM) and lactogen (150 +/- 14 pg/g) receptors were unchanged after training. However, the capacity of testicular interstitial cell suspensions to produce cAMP and testosterone increased by 20-30% during in vitro gonadotropin stimulation. In the second part, the trained and untrained control animals underwent acute exhaustive exercise. Serum testosterone levels decreased by 74 and 42% in trained and untrained rats, respectively (P less than 0.02), and corticosterone rose by 182% in trained and 146% in untrained rats (P less than 0.01), whereas the LH level was unchanged. Testicular levels of testosterone and its precursors decreased, with the exception of unchanged androstenedione, in trained rats; the cAMP concentration was unchanged. In both trained and untrained rats, acute exercise decreased the capacity of interstitial cell suspensions to produce cAMP, whereas there were no consistent effects on testosterone production. Acute exercise had no effect on LH or lactogen receptors in testis tissue. In conclusion, training had no effect on serum or testicular androgen concentrations, but increased Leydig cell capacity to produce testosterone and cAMP. Acute exercise decreased serum and testicular testosterone concentrations without affecting serum LH. A direct inhibitory effect of the increased serum corticosterone level on the hypothalamic-pituitary level and/or testis may be the explanation for this finding.     

Chronic administration of corticosterone impairs LH signal transduction and steroidogenesis in rat Leydig cells

The mechanism involved in the inhibitory actions of chronic corticosterone treatment on Leydig cell steroidogenesis was studied in adult Wistar rats. Rats were treated with corticosterone-21-acetate (2 mg/100 g body weight, i.m., twice daily) for 15 days and another set of rats was treated with corticosterone plus ovine luteinizing hormone (oLH) (100 microg/kg body weight, s.c., daily) for 15 days. Chronic treatment with corticosterone increased serum corticosterone but decreased serum LH, testosterone, estradiol and testicular interstitial fluid (TIF) testosterone and estradiol concentrations. Administration of LH with corticosterone partially prevented the decrease in serum and TIF testosterone and estradiol. Leydig cell LH receptor number, basal and LH-stimulated cAMP production were diminished by corticosterone treatment which remained at control level in the corticosterone plus LH treated rats. Activities of steroidogenic enzymes, 3beta- and 17beta-hydroxysteroid dehydrogenase (3beta-HSD and 17beta-HSD) were significantly decreased in corticosterone treated rats. LH plus corticosterone treatment did not affect 3beta-HSD activity but decreased 17beta-HSD activity, indicating a direct inhibitory effect of excess corticosterone on Leydig cell testosterone synthesis. The indirect effect of corticosterone, thus, assume to be mediated through lower LH which regulates the activity of 3beta-HSD. Basal, LH and cAMP-stimulated testosterone production by Leydig cells of corticosterone and corticosterone plus LH treated rats were decreased compared to control suggesting the deleterious effect of excess corticosterone on LH signal transduction and thus steroidogenesis.     

Corticosterone treatment has no effect on reproductive hormones or aggressive behavior in free-living male tree sparrows, Spizella arborea

We examined the effect of corticosterone on plasma levels of reproductive hormones (testosterone, dihydrotestosterone, and luteinizing hormone) and territorial defense behavior in male tree sparrows, Spizella arborea. Birds receiving Silastic implants filled with corticosterone (B) had significantly higher plasma levels of B than control birds, which received empty implants, and exhibited pectoral muscle wastage and a decrease in body mass. We evaluated the hormonal and agonistic responses of the two implanted groups of birds using a simulated territorial intrusion (STI) 2 to 4 days after they were implanted. Corticosterone-treated and control birds did not differ in their circulating levels of reproductive hormones or in their behavioral responses to STI (latency to respond to intrusion, number of songs, and closest approach to a decoy and tape recording). Unlike previous studies of north temperate passerines, high physiological levels of exogenous B had no effect either on circulating levels of reproductive hormones or on territorial behaviors associated with breeding. Nonetheless, untreated tree sparrows do mount a robust adrenocortical response, having a two- to fourfold increase in plasma B levels during a 1-h period of capture. Thus, adrenocortical responsiveness is maintained in these birds, but elevated levels of glucocorticoids do not suppress reproductive hormones or associated behaviors. We believe that this hormonal and behavioral refractoriness to glucocorticoids-or uncoupling of the stress response from the reproductive axis-may be advantageous for species having extreme temporal constraints on their breeding schedules.     

Extraocular control of photorefractoriness in American tree sparrows (Spizella arborea)

Photorefractoriness, a reversible state of unresponsiveness to daylengths of gonadostimulatory duration, terminates seasonal breeding in many photoperiodic species of birds. Whether the eyes are components of the mechanism that triggers photorefractoriness is an important, but heretofore unresolved, question. Although a role for extraocular photoreception in the mechanism of photoinduced gonadal growth is well documented, the eyes may be important in the mechanism of photorefractoriness if, as some evidence suggests, they are gonadoinhibitory. With American tree sparrows (Spizella arborea), I here confirm that the absence of eyes does not impede photoinduced testicular growth and establish that an extraocular mechanism mediates the transition from photosensitivity to photorefractoriness: Tree sparrows blinded by bilateral ocular enucleation, when photosensitivity to long days or by miniature self-powered lights implanted atop the skull, showed marked testicular growth and then, as evidenced by spontaneous testicular regression, became photorefractory, as did sighted controls.     

Interrelationships between the hypothalamus, pituitary gland, ovary, adrenal gland, and the open period for LH release in the hen (Gallus domesticus)

The asynchronous ovulatory cycle of the hen is believed to be the consequence of two interacting systems, one of which is circadian and regulates the timing of the preovulatory LH surge. In support of this proposition, the open period for LH release was shown to oscillate with the same periodicity as the photoschedule when the hens were exposed to 14 L:7 D, 14 L:10 D, and 14 L:14 D. In addition, it was demonstrated that follicular maturation is not affected by or synchronized with the photoperiod. The physiological system that transduces the light/dark cycle into an open period for LH release has not been identified although circumstantial evidence supports the idea that the adrenal gland plays a role in this function. This evidence includes the anatomical juxtaposition of the left ovary and adrenal gland, innervation of steroid-producing cells within the follicle by nerve tracts passing through the adrenal glands, the ability of injections of metyrapone to alter the timing of preovulatory LH release, the ability of injections of corticosterone to induce ovulation when a mature follicle is present in the ovary, and the ability of dexamethasone or infusions of corticosterone to block ovulation. Recently we have also shown that infusions of corticosterone will block the gonadotropic effect of PMSG, will inhibit the photoperiodic response, and do not affect the release of LH in response to injections of GnRH. The addition of corticosterone to incubations of dispersed granulosa cells does not affect their response to LH. These data suggest that corticosterone may modulate the responsiveness of the hypothalamus to tropic stimuli and demonstrate that exposure to corticosterone can alter the responsiveness of some ovarian tissues to gonadotropins.     

Photoperiodically-induced changes in hypothalamic-pituitary-adrenal axis sensitivity in captive house sparrows (Passer domesticus)

We used captive house sparrows (Passer domesticus) to identify regulatory mechanisms underlying seasonal (mimicked by changes in photoperiod) and diel differences in corticosterone output. Corticosterone responses were measured during three simulated seasons: short-day and long-day photoperiods and while birds underwent a pre-basic molt. Under all three conditions we tested for adrenal sensitivity by injecting exogenous ACTH, for pituitary sensitivity by injecting corticotropin-releasing factor (CRF) and arginine vasotocin (AVT), and for diel changes by repeating the injections during the day and at night. The daytime adrenal sensitivities were greatest on long days, lower on short days, and lowest during molt. These data suggest that reductions in either adrenal sensitivity to ACTH and/or capacity to secrete corticosterone could explain lowered endogenous corticosterone titers during molt. Furthermore, adrenal sensitivity to ACTH and pituitary sensitivity to AVT appeared to be greatest at night. This suggests that both the adrenal's sensitivity to the ACTH signal and the pituitary's capacity to secrete ACTH might provide a mechanism allowing for diel changes in corticosterone titers. This differs substantially from what is known about diel regulation in rodents. Taken together, these data provide further evidence that there are complex regulatory mechanisms controlling diel and seasonal changes in corticosterone titers in birds.     

Chronic corticosterone treatment impairs Leydig cell 11beta-hydroxysteroid dehydrogenase activity and LH-stimulated testosterone production.

The effects of excess corticosterone on luteinizing hormone (LH)-stimulated Leydig cell testosterone production and activity of 11beta-HSD was studied. Adult male rats (200-250 g body weight) were treated with corticosterone-21-acetate (2 mg/100 g body weight, i.m., twice daily) for 15 days. Another set of rats was treated with corticosterone (dose as above) plus LH (ovine LH 100 microg/kg body weight, s.c., daily) for 15 days. Corticosterone administration significantly increased serum and testicular interstitial fluid (TIF) corticosterone but decreased testosterone levels. Administration of LH with corticosterone partially prevented the decrease in serum and TIF testosterone. The oxidative activity of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) was significantly decreased in Leydig cells of rats treated with corticosterone alone and in combination with LH. The direct effect of corticosterone on Leydig cell steroidogenic potency was also studied in vitro. Addition of corticosterone to Leydig cell culture showed a dose dependent effect on LH-stimulated testosterone production. Corticosterone at 50 and 100 ng/ml did not alter LH-stimulated testosterone production, but at high doses (200-400 ng/ml), decreased basal and LH-stimulated testosterone production. Basal and LH-stimulated cAMP production was not altered by corticosterone in vitro. It is concluded from the present study that elevated levels of corticosterone decreased the oxidative activity of 11beta-HSD and thus resulting in impaired Leydig cell steroidogenesis and the inhibitory effects of corticosterone on testosterone production appear to be mediated through inhibition of LH signal transduction at post-cAMP level.     

Diurnal Sensitivity of the Neuroendocrine-Reproductive Axis to the Antigonadotrophic Influence of Melatonin in Male Syrian Hamsters with Experimentally Altered Cortisol Rhythms

Two different experimental models were used to test if a temporal relationship exists between the rhythm of adrenal steroid secretion and the vulnerability of the hamster reproductive system to short photoperiod exposure or to the daily afternoon injection of melatonin. In the first experiment adrenalectomized hamsters were implanted with a Cortisol pellet to provide a sustained, rather than rhythmic, level of the hormone. The animals were either placed in short photoperiod or given a daily afternoon melatonin injection. In both cases the gonads underwent atrophy. In the second experiment adrenalectomized hamsters were given a Cortisol injection either in the morning (approx. 8 hr before the subsequent afternoon injection of melatonin) or in the afternoon (approx. 1 hr before the subsequent melatonin injection). Measurements of testicular and accessory organ weights 7 weeks later indicated regression of the reproductive system in both the groups when compared with their appropriate controls. Depressed levels of plasma LH. PRL, testosterone and thyroxine (T4) in these animals confirmed the melatonin induced gonadal collapse. The results suggest that apparently there is no temporal correlation between the rhythm of secretion of the adrenal steroids and the responsiveness of the reproductive system to late afternoon injection of melatonin. Interestingly, all the adrenalectomized Cortisol injected control animals (not receiving melatonin) had depressed plasma LH and PRL while the testicular weights and plasma testosterone titers remain unaffected.     

Influence of melatonin on the testicular regression induced by subcutaneous testosterone pellets in male rats kept in long or short photoperiod

Daily afternoon injections of 25 micrograms melatonin for 12 weeks had no effect on testicular weights of male rats kept in long photoperiod (14L:10D); similarly, exposure of rats to short photoperiod (2L:22D) had no effect on gonadal weight. However, rats maintained in a long or short photoperiod and implanted every 2 weeks with a 15 mm Silastic pellet containing testosterone showed a significant reduction in testicular weight; this effect was more pronounced in rats exposed to a short photoperiod. Melatonin injections in testosterone-treated rats in a long photoperiod exacerbated the inhibitory effects of testosterone alone. Subcutaneous 2-weekly implants of a beeswax pellet containing 1 mg melatonin reversed the effects of the melatonin injections on relative testicular weights but not those due to short photoperiod exposure. Testosterone implants significantly reduced pituitary LH values in long and short photoperiod-exposed animals, more particularly in those exposed to short photoperiod. Melatonin injections alone or in combination with melatonin pellets did not further exaggerate the depression in pituitary LH due to testosterone alone in long photoperiod-exposed animals; similarly melatonin pellets did not reverse the depression in pituitary LH observed. No significant differences in plasma prolactin concentrations or in thyroxine concentrations or free thyroxine index were observed after any combination of treatments. We therefore suggest that the effects observed with short photoperiod may be due to melatonin.     

The thyroid and photoperiodic control of seasonal reproduction in American tree sparrows (Spizella arborea)

To explore the role of the thyroid gland in the control of seasonal reproduction in obligately photoperiodic American tree sparrows (Spizella arborea), the effects of (1) thyroxine administered in drinking water to thyroid-intact photosensitive or photorefractory birds, and (2) radiothyroidectomy before and after photostimulation and during photorefractoriness were examined. Chronic administration of pharmacological doses of thyroxine induced testicular growth and usually regression in initially photosensitive birds held on short or intermediate daylengths. Some thyroxine-treated birds with regressed testes were absolutely photorefractory, but most remained photosensitive. Exogenous thyroxine never induced testicular growth in photorefractory birds moved to short days, though it often impeded, and sometimes even blocked, the recovery of photosensitivity. Although circumstantial, these effects of exogenous thyroxine are consistent with an hypothesis that assigns to thyroid hormones two roles — one stimulatory and the other inhibitory — in the control of seasonal reproduction. Radiothyroidectomy before photostimulation inhibited (but did not prevent) photoinduced testicular growth, blocked spontaneous testicular regression, suppressed molt, and prevented photorefractoriness. Moreover, as demonstrated by testicular growth after thyroxine replacemnt therapy, radiothyroidectomy during photorefractoriness later restored photosensitivity despite continued photostimulation. Thus, euthyroidism is an essential condition for maximizing (but not for initiating) photoinduced testicular growth and for triggering and maintaining photorefractoriness in photostimulated tree sparrows. However, when performed early during photostimulation, radiothyroidectomy neither immediately induced nor later blocked spontaneous testicular regression. Thus, endogenous thyroid hormones and long days may interact during a critical period to program a sequence of physiological events that plays out as photorefractoriness in chronically photostimulated birds. Such an organizational event cannot be permanent, for seasonal reproduction is episodic and its control mechanism necessarily cyclic. Because thyroidectomy simulated the well-known restorative effect of short days (and exogenous thyroxine impeded it), short days may dissipate photorefractoriness by creating a milieu wherein thyroid hormones are deficient or inactive.Abbreviations ANOVA analysis of variance - bTSH bovine thyroid stimulating hormone - GnRH gonadotropin-releasing hormone - LH luteinizing hormone - nL: nD daily light: dark regime (n is duration in hours) - SEM standard error of the mean - SNK Student-Newman-Keuls test - T₄ thyroxine - TH thyroid hormone - TR thyroid hormone receptor     

Relative photorefractoriness, prolactin, and reproductive regression in a flexibly breeding sonoran desert passerine, the rufous-winged sparrow, Aimophila carpalis

We tested the hypothesis that adult male rufous-winged sparrows, Aimophila carpalis, exhibit relative photorefractoriness. This condition results in partial loss of sensitivity to photoperiod as a reproductive stimulus after prolonged exposure to long photoperiods and is similar to the mammalian condition called photoperiodic memory. Captive birds were exposed either to 8 h of light/16 h of dark per day (8L) or to 16L for 11 weeks and were then exposed either to 8L, 13L, 14L, or 16L. Testicular diameter, plasma luteinizing hormone (LH), and plasma prolactin (PRL) were measured to assess reproductive system activity in response to photostimulation. In free-living birds, testicular diameter, plasma LH, and PRL were compared in birds caught in September in a year when birds were breeding and in a year when birds were not breeding to further evaluate the role of PRL in the termination of seasonal breeding. Testes completely developed after transfer from 8L to 14L or to 16L and partially developed after transfer from 8L to 13L. However, after 11 weeks of 16L exposure, transfer to 14L caused partial regression and transfer to 13L caused complete regression of the testes. Plasma LH increased in all birds that were transferred from 8L to a longer photoperiod. PRL showed a weak response to longer photoperiod treatment and was elevated in birds after chronic 16L exposure in comparison to birds exposed to chronic 8L. These data indicate that male rufous-winged sparrows lose sensitivity to photoperiod after long photoperiod exposure consistent with the relative photorefractoriness and photoperiodic memory models. Lower PRL in birds that developed testes on 13L and 14L compared to birds that regressed testes on 13L and 14L are consistent with the hypothesis that PRL regulates relative photorefractoriness. However, PRL does not appear to regulate interannual differences in the timing of testicular regression.     

Excessive dietary calcium in the disruption of structural and functional status of adult male reproductive system in rat with possible mechanism

Calcium is essential for functioning of different systems including male reproduction. However, it has also been reported as chemo-castrative agent. The study has been undertaken to elucidate the effect of excessive dietary calcium on male reproductive system in animals with possible action. Adult male healthy rats fed CaCl(2) at different doses (0.5, 1.0 and 1.5 g%) in diet for 13 and 26 days to investigate reproductive parameters as well as the markers of oxidative stress. Significant alteration was found (P < 0.05) in testicular and accessory sex organs weight, epididymal sperm count, testicular steroidogenic enzyme (Δ(5) 3β-HSD and 17β-HSD) activities, serum testosterone, LH, FSH, LPO, activities of antioxidant enzymes, testicular histoarchitecture along with adrenal Δ(5) 3β-HSD activity with corticosterone level in dose- and time-dependent manner. Overall observations suggest that excessive dietary calcium enhances the generation of free-radicals resulting in structural and functional disruption of male reproduction.     

The systemic response of male mice to differential housing: A path-analytical approach

Path analysis was used to examine the effects of grouping/individual housing, duration of differential housing (13 days or 10 weeks), and the age at which differential housing was initiated (at weaning or 4 months) on the physiology of male TT strain mice. Variables studied included body and relative ventral prostate, left testis and left adrenal gland weights, and plasma corticosterone level and (Na+) /(K+) ratio. Compared with grouped counterparts, individual housing produced lower adrenal weights and plasma corticosterone levels, but higher prostate weights. This housing condition also suppressed the plasma (Na+)/(K+) ratio, probably through an action on aldosterone secretion. The adrenal response to differential housing thus appears to be at a number of levels, involving at least two separate components. No evidence was found to support the notion that the gonadal response to grouping is mediated via the adrenal gland, although prolonged grouping does generate reduced testicular weights.     

24-hour changes in ACTH, corticosterone, growth hormone, and leptin levels in young male rats subjected to calorie restriction

Calorie restriction of young male rats increases plasma prolactin, decreases luteinizing hormone (LH) and testosterone, and disrupts their 24 h secretory pattern. To study whether this could be the consequence of stress, we examined the 24 h variations of plasma adrenocorticotropic hormone (ACTH) corticosterone, growth hormone (GH), leptin, and adrenal corticosterone. Rats were submitted to a calorie restriction equivalent to a 66% of usual intake for 4 weeks, starting on day 35 of life. Controls were kept in individual cages and allowed to eat a normal calorie regimen. Significantly lower ACTH levels were detected in calorie-restricted rats. Plasma corticosterone levels during the light phase of the daily cycle were significantly higher in calorie-restricted rats. Time-of-day variation in plasma ACTH and corticosterone levels attained significance in calorie-restricted rats only, with a maximum toward the end of the resting phase. The daily pattern of adrenal gland corticosterone mirrored that of circulating corticosterone; however, calorie restriction reduced its levels. Plasma ACTH and corticosterone correlated significantly in controls only. Calorie restriction decreased plasma GH and leptin, and it distorted 24 h rhythmicity. In a second study, plasma ACTH and corticosterone levels were measured in group-caged rats, isolated control rats, and calorie-restricted rats during the light phase of the daily cycle. Plasma ACTH of calorie-restricted rats was lower, and plasma corticosterone was higher, compared with isolated or group-caged controls. The changes in the secretory pattern of hormones hereby reported may be part of the neuroendocrine and metabolic mechanisms evolved to maximize survival during periods of food shortage.     

The differential effect of atrazine on luteinizing hormone release in adrenalectomized adult female Wistar rats

High doses of atrazine (ATR), administered for 4 days, suppress luteinizing hormone (LH) release and increase adrenal hormones levels. Considering the known inhibitory effects of adrenal hormones on the hypothalamo-pituitary-gonadal axis, we investigated the possible role the adrenal gland has in mediating ATR inhibition of LH release. To determine the extant and duration of adrenal activation, ovariectomized Wistar rats were given a single dose of ATR (0, 50, or 200 mg/kg), and corticosterone (CORT) levels were assayed at multiple time points posttreatment. CORT levels were increased within 20 min and remained elevated over 12 h postgavage in 200-mg/kg animals. To determine the effects of adrenalectomy on ATR inhibition of the LH surge and pulsatile LH release, adrenalectomized (ADX) or sham-operated ovariectomized rats were treated for 4 days with ATR (0, 10, 100, or 200 mg/kg), and an LH surge was induced with hormone priming. In the afternoon following the last dose of ATR, blood was sampled hourly for 9 h. Another cohort of ovariectomized rats was examined for pulsatile patterns of LH secretion after ATR (0, 50, or 200 mg/kg) and sampled every 5 min for 3 h. ADX had no effect on ATR inhibition of the LH surge but prevented the ATR disruption of pulsatile LH release. These data indicate that ATR selectively affects the LH pulse generator through alterations in adrenal hormone secretion. Adrenal activation does not play a role in ATR's suppression of the LH surge, and therefore ATR may work centrally to alter the preovulatory LH surge in female rats.     

Effects of diethylstilboestrol on testicular function and luteinizing hormone receptors

Adult male Fisher-344 rats were implanted with DES-filled or empty Silastic capsules. After 14 weeks, capsules were removed and a second group of rats received DES capsules. Seven weeks later, all the rats were sacrificed. DES treatment decreased body, testes and seminal vesicle weights, and removal of the capsules partially restored the weight of these organs. The concentration of testicular LH receptors was increased by DES treatment. Circulating PRL levels were increased and gonadotropin levels were reduced in all animals having received DES at anytime. Plasma testosterone (T) levels were similar in all groups, but testicular T levels were reversibly decreased by DES. Similarly, whereas basal incubation media T levels were unchanged by DES treatment, the steroidogenic response in vitro to hCG was abolished by the presence of DES, and removal of the capsules restored this response. It appears that in this animal model DES and PRL exert opposing effects on testicular LH receptor.     

A test of the hypothesis that T3 is the "seasonality" thyroid hormone in American tree sparrows (Spizella arborea): intracerebroventricular infusion of iopanoic acid, an inhibitor of T3 synthesis and degradation

This study tested the hypothesis that L-3,5,3'-triiodothyronine (T3) is the bioactive "seasonality" thyroid hormone in American tree sparrows (Spizella (arborea). The experimental approach coupled thyroid hormone replacement therapy after radiothyroidectomy with photostimulation and intracerebroventricular infusion of iopanoic acid, an inhibitor of L-3,5,3'-triiodothyronine synthesis and degradation. Endpoints were testis length, molt score, and hypothalamic content of chicken gonadotropin-releasing hormone 1. The hypothesis predicts that thyroidectomized male tree sparrows moved to long days and given thyroxine in combination with iopanoic acid will lack L-3,5,3'-triiodothyronine and so will not express thyroid hormone-dependent photoperiodic testicular growth (a vernal component of seasonality) and photorefractoriness or postnuptial molt (autumnal components of seasonality). It further predicts that iopanoic acid will enhance the efficacy of L-3,5,3'-triiodothyronine and so will facilitate the expression of seasonality in thyroidectomized males given L-3,5,3'-triiodothyronine replacement therapy. Iopanoic acid had no significant effect on any component of seasonality in thyroid-intact males given vehicle, or in thyroidectomized males given thyroxine or L-3,5,3'-triiodothyronine. Thyroid-intact males, as well as thyroidectomized males infused with thyroxine alone, commonly expressed all components of seasonality. Thyroidectomized males given L-3,5,3'-triiodothyronine alone exhibited photoperiodic testicular growth, but did not become photorefractory or initiate molt. While these results confirm that thyroid hormone acts centrally to program American tree sparrows for seasonality, they do not support the hypothesis that L-3,5,3'-triiodothyronine is the bioactive "seasonality" thyroid hormone, and they challenge the view that thyroxine is merely a prohormone.     

Role of glucocorticoids in the stress-induced suppression of testicular steroidogenesis in adult male rats.

We have examined the role of glucocorticoids in the stress-induced inhibition of testicular steroidogenesis. Immobilization (3 hr) reduced plasma testosterone (T) levels to 24% of control values but did not affect plasma LH levels. This reduction was partially reversed by in vivo injections of the antiglucocorticoid, RU486, prior to the stress session at a dose of 10 mg/kg BW, but not at 1.0 or 50 mg/kg BW. Stressed rats that were treated with 10 mg/kg BW RU486 had twofold higher plasma T levels than vehicle-treated stressed animals. Injections of RU486 did not affect plasma LH levels in control or stressed rats and did not affect T levels of unstressed rats. Stressed rats had eightfold higher plasma corticosterone levels than controls, and RU486 had no effect on control or stress levels of corticosterone. The possible role of glucocorticoids in mediating the effect of stress on testicular T production was investigated also in vitro by incubating testicular interstitial cells from unstressed rats for 3 hr with corticosterone (0, 0.01, 0.1, or 1.0 microM) or dexamethasone (0, 0.001, 0.01, or 0.1 microM), followed by an additional 2 hr with hCG (0, 25, 50, or 100 microIU). Both corticosterone and dexamethasone inhibited hCG-stimulated T production in a dose-dependent manner. Cells incubated with the highest concentration of either of the glucocorticoids showed significantly reduced responses to hCG stimulation. In the absence of hCG, in vitro T production was not affected by dexamethasone or 0.01 and 0.1 microM corticosterone. However, the highest dose of corticosterone (1.0 microM) produced a 63% elevation in basal T production. Coincubation of testicular interstitial cells with corticosterone (1.0 microM) or dexamethasone (0.1 microM) and RU486 (0.01, 0.1, and 1.0 microM) reversed the glucocorticoid-induced suppressions of T production in a dose-dependent manner. Our results suggest that during stress increases in plasma levels of glucocorticoids in male rats act via glucocorticoid receptors on testicular interstitial cells to suppress the testicular response to gonadotropins, and that the decline of testosterone production during immobilization stress is in part mediated by a direct action of glucocorticoids on the testis.     

Influence of adrenal cortex on testicular activity in the toad during the breeding season

The aim of the present study was to determine the role of adrenals in gonadal activity in the male toad during the breeding season. Exogenous administration of corticosterone or metapyrone for 6 days inhibited adrenal delta5-3beta(delta 5-3 beta) hydroxysteroid (delta5-3beta-HSD) and testicular 17beta (17 beta) hydroxysteroid dehydrogenase (17beta-HSD) activities, decreased the serum levels of testosterone and inhibited spermatogenesis. When toads were treated with corticosterone a significant rise of serum corticosterone was noted while metapyrone treatment appeared to decrease serum corticosterone levels. It is concluded that adrenocortical hormone plays an indirect role in testicular activity in toads during the breeding season.