The sexual system of fetal and adult male rats of 2 strains after prenatal exposure to glucocorticoids

Testosterone level in male fetuses and adults after glucocorticoid injection to their mothers on 16-th and 18-th days of pregnancy as well as morphometric characteristics of male adult reproductive system of two outbred strains (aggressive and domesticated) were investigated. Prenatal hormonal treatment resulted in genotype-dependent changes in testosterone level in 21-day-old male fetuses; it was decreased in fetuses of domesticated rats and increased in fetuses of aggressive rats. The direction of these changes coincided completely with the subsequent changes in relative weight of preputial gland and seminal vesicles in adults. Thus, the level of glucocorticoids during prenatal period plays an important role in reproductive system development and the character of the action depends on the genotype.     

Sexual behavior in developing male rats

During normal development, the onset of reproductive behavior in male rats was not preceded by any change in plasma testosterone (T) levels. Implantation of Silastic capsules containing T in 14-day-old male rats advanced the onset of all parameters of sexual behavior by 20 days. Implantation of Silastic capsules containing estradiol in 14-day-old male rats stimulated precocious mounting and intromitting, but not ejaculation. Implantation of dihydrotestosterone-filled Silastic capsules in 14-day-old male rats completely inhibited the development of sexual behavior. All hormones suppressed plasma LH levels. These findings in immature male rats are similar to previous findings in adult males. Immature male rats were behaviorally less responsive to T than adult males, and it was suggested that, during development, male rats become progressively more sensitive to the behavior-stimulating effects of circulating T. No effects of copulatory experience on plasma concentration of T or on the weights of testes, penes, or accessory sexual glands were detected.     

Naloxone stimulation of luteinizing hormone release in prepubertal female rats; role of serotonergic system

The purpose of this study was to determine whether naloxone stimulated LH release via a serotonergic mechanism. Injection of naloxone hydrochloride (2 mg/kg B.W.) into 25-day old female prepubertal rats resulted in a significant elevation in serum LH 30 min later. Injection of this dose of naloxone together with morphine sulfate (2 or 5 mg/kg B.E.) resulted in inhibition of naloxone-induced LH release. When rats were first injected with 5-hydroxytryptophan (5-HTP) to increase hypothalamic serotonin content, naloxone failed to increase serum LH levels. On the other hand, when parachlorophenylalanine (PCPA) was given first to reduce hypothalamic serotonin content, naloxone-induced LH release was potentiated. Morphine failed to inhibit the naloxone-induced rise in serum LH when PCPA was first administered. Neither 5-HTP nor PCPA, when injected alone, altered serum LH values. These results suggest that naloxone promotes LH release by reducing hypothalamic serotonergic activity, and morphine inhibits LH release by increasing hypothalamic serotonergic activity. This does not exclude possible involvement of other neurotransmitters.     

Altered sexual differentiation of hepatic uridine diphosphate glucuronyltransferase by neonatal hormone treatment in rats

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.     

Brain serotonin in response to the hypothalamo-hypophyseal-adrenal system to insulin hypoglycemia

The response of hypothalamus-pituitary-adrenal system to insulin administration was studied in the male Wistar rats submitted to a strong and prolonged blockade of serotonin brain synthesis by repetitive injections of p-chlorophenylalanine (PCPA) a 5-hydroxytryptophan inhibitor. After 24, 48, 72 or 96 hours of either one or two doses of PCPA (250 mg/kg, i.p.) were administered with insulin (0.25 UI/kg s.c.), the plasmatic glucose and corticosterone levels being estimated at 0, 30 and 60 minutes. When PCPA was injected twice, the lapse between them was 48 hours. Insulin produced decrease of plasmatic corticosterone values and inhibition of the response to insulin, specially between 48 and 72 hours, for a single management of PCPA, and stronger and more prolonged for the double dose. The fall of serotonin content in brain maintained great correlation with effects referred above. The results support that stimulatory action of insulin on the pituitary-adrenal system is mediated by central serotoninergic neurons and reaffirms the hypothesis that serotonin (5HT) positively modulates the activity of hypothalamus-pituitary-adrenal system.     

The effects of testosterone and estrogen on the pituitary growth hormone response to growth hormone-releasing factor

The effects of testosterone and estrogen on the pituitary growth hormone response to hypothalamic growth hormone-releasing factor (GRF) were evaluated in vivo using male and female rats and in vitro using a pituitary cell monolayer culture system. In vivo the increase in plasma growth hormone (GH) concentration in response to a 500 ng/kg dose of GRF was similar in gonadectomized male and female rats. Pretreatment of intact and gonadectomized male rats with testosterone caused significant enhancement of the pituitary GH response to GRF, whereas pretreatment of gonadectomized female rats with 17 beta-estradiol did not alter the response. The GH response to GRF was not different between prepubertal (i.e., 30-day-old) male and female rats. However, following puberty (i.e., by 60 days of age), the response in male rats was significantly greater than that observed in female rats. The in vitro preincubation of anterior pituitary cells with either testosterone or 17 beta-estradiol did not cause any shift in the dose-response curve between GRF and GH. These results demonstrated that androgens play an active role in modulating the pituitary response to GRF in vivo.     

Ca2+-dependent secretion of serotonin by the rat hypothalamus during ontogenesis

A study was made of functional maturity of the terminal part of serotoninergic system of rat hypothalamus in perinatal period: the maturity was estimated by the ability to release serotonin. The release of specifically taken up serotonin (3H-5-OT) by the tissue of hypothalamus of 16-20-day-old rat fetuses, 8-9-day males and adult males was studied in the perfusion system. Spontaneous release of the labelled amine was recorded in the earliest studied period--on the 16th day of the prenatal period, but the response to K+ depolarization was absent at this time. For the first time the increase of the rate of 3H-5-OT release in response to depolarization was noted on the 17th day of development. In the absence of Ca2+ depolarizing stimulus produced no increase in the release of the labelled product. Similar results were obtained with perfusion of fetal hypothalamus on the 18t hand 20th days of development. In neonatal animals the release of 5-OT in response to depolarization was equal to that in adults. The data obtained point to a possible functioning of serotoninergic elements of hypothalamus in the perinatal period in rats.     

Serotonin involvement in the inhibition of luteinizing hormone (LH) release during immobilization in castrated male rats

The involvement of serotonin in mediating the inhibitory effect of immobilization stress on LH secretion in castrated male rats was examined by employing p-chlorophenylalanine (PCPA, 320 mg/kg, ip), an inhibitor of serotonin synthesis, and 5,6-dihydroxytryptamine (5,6-DHT, 50 micrograms, icv), a drug toxic to the indoleaminergic system. Immobilization stress suppressed pulsatile LH release and decreased mean plasma LH levels. Pretreatment with PCPA or 5,6-DHT apparently eliminated the inhibitory effect of immobilization stress on LH release. These results suggest the possible involvement of a serotoninergic mechanism in mediating the suppression of LH release induced by immobilization stress in castrated male rats.     

Antiandrogenic effect of perinatal exposure to the endocrine disruptor di-(2-ethylhexyl) phthalate increases anxiety-like behavior in male rats during sexual maturation

Di-2-ethylhexyl phthalate (DEHP) is the most widely used phthalate to convey flexibility and transparency to plastic products made of polyvinyl chloride. It has been recognized as endocrine disruptor and associated with reproductive toxic effects. We examined the effects of perinatal exposure to DEHP on anxiety-like behavior, using the Elevated Plus Maze (EPM) test, in male and female rats at different stages of sexual development. Anxiety-like behavior was expressed as a) frequency of open arm entries over the total arm entries (% FEO); b) time spent in them compared with total time the animal stayed in the EPM (% TSO) and c) time spent in closed arms (TSC). Because DEHP has anti-androgenic action we also tested control and exposed immature male rats pretreated with testosterone. We found sex differences in behavior induced by DEHP; while male rats of 45 and 60 days of age showed a significant decrease in FEO and TSO percentages, as well as an increase in TSC, no changes were observed in anxiety-like behavior in perinatal DEHP exposed females at these ages of sexual maturation. In 60-day-old male rats, DEHP exposure produced a significant decrease in serum testosterone levels. Testosterone replacement was able to antagonize the adverse effects of DEHP exposure on LH, activating the negative feed-back mechanism of this steroid on reproductive axis, as well as increasing FEO and TSO percentages to similar values observed in the control group. These findings suggest that the anti-androgenic action of this chemical could be one possible mechanism underlie anxiogenic-like behavior produced by perinatal DEHP exposure in 60-day-old male rats.     

Effects of prepubertal manipulation with androgens on the development of sexual differences in the harderian glands of Syrian hamsters.

The onset of sexual differences in the metabolism of porphyrins and melatonin in the Harderian glands of Syrian hamsters was studied. Three weeks after birth, the porphyrin concentrations were already higher in glands of females than in those of males. Castration of 22-day-old male hamsters led to an increase in Harderian porphyrin concentrations, although the levels of intact females were not reached. The administration of testosterone to 22-day-old female hamsters resulted in a marked decrease in porphyrin concentrations. Study of the development of sexual differences in the enzymes involved in melatonin synthesis, N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT) indicated that not all the sexual differences observed in these glands begin at the same time. Thus, while differences in NAT activity were detected after the age of 3 weeks, male-female differences in HIOMT activity were only observed after 7 weeks. Castration of prepubertal male hamsters lowered NAT but not HIOMT activities. The administration of testosterone to prepubertal female hamsters led to male activity levels in both enzymes. Although circulating androgens seem to have a crucial role in maintaining sexual differences, other hormones including those from the pituitary and thyroid glands are probably also important for generating these sexual differences.     

Hypothalamic excitatory amino acid system during sexual maturation in female rats

The present results indicate that during sexual maturation the APOA-MBH from rats of 30 days of age released significantly higher quantities of GnRH than the tissue from 16-day-old rats (P < 0.01). The addition of NMDA, an agonist of the excitatory amino acids system (EAAs), to the medium after 30 min of incubation significantly increased (P < 0.01) the GnRH release in normal rats of both ages and this increase was significantly (P < 0.01) higher in 30-day-old rats (to 661%) than in rats of 16 days of age (to 273%). The administration of estrogen-progesterone (EP) to rats of 16 days of age did not modify the GnRH release response to NMDA. On the contrary, at 30 days of age EP administration significantly potentiated the GnRH release response to NMDA since while in the control group NMDA increased the GnRH release to 630%, in the EP-pretreated group this was to around 4700% (P < 0.01). EP pretreatment of prepubertal rats decreases the hypothalamic release of aspartate and glutamate, the excitatory amino acids involved in NMDA neurotransmission and glycine but increases EAAs release in peripubertal rats. On the basis of these results it is proposed that the increase in EAAs release by the hypothalamus is directly connected with the onset of puberty and that the maturation of the positive feedback effect of ovarian hormones on gonadotropin secretion is related to the maturation of the capacity of EP to increase hypothalamic EAAs. Before this maturational event EP inhibits EAAs release as well as gonadotropin release (prepubertal rats). NMDA receptor stimulation leads to a positive mechanism which increases the release of Asp and Glu from APOA-MBH both in prepubertal and peripubertal rats, but EP potentiates this mechanism only in peripubertal rats. This could be an additional neuroendocrine mechanism involved in the increase of gonadotropin during sexual maturation which induces the onset of puberty and the preovulatory discharge of these pituitary hormones.     

A quantitative study of serum testosterone,sex accessory organ growth,and the development of intermale aggression in the mouse

Radioimmunoassay of serum testosterone (T) was used to characterize circulating T levels in mice from birth to sexual maturity. Until 25 days of age, serum T levels ranged from 1 to 4 ng/ml. A significant increase in T concentrations was observed in 30-day-old males, followed by a secondary rise in serum T between Days 45 and 50 of life. The latter increment was associated with the appearance of extreme individual variation in circulating T levels which was also observed in adult (120 days) males. The most rapid growth of accessory sex organs occurred between 30 and 50 days of age, the period preceding attainment of peak serum-T levels. The first incidence of intermale aggression coincided with a prepubertal rise in circulating T, but adult levels of fighting were present prior to the secondary increase in T observed between 45 and 50 days of age. Although animals involved in a fight did not differ with respect to weight of the accessory sex organs or serum T concentrations, the male that weighed more than his opponent usually won an encounter. Compared to males in encounters in which no fighting occurred, animals that won or lost an aggressive encounter showed significantly greater accessory sex organ development. While circulating T is required for the initiation and maintenance of intermale aggression, it is apparent that additional factors are related to the onset of fighting and the establishment of dominance/ subordinance relationships in mice.     

Effect of ethanol in preovulatory periods on LH, FSH, prolactin and ovulation in rats

The effect of ethanol (4 g/kg) as well as the role of serotoninergic neurons on the rate of ovulation and plasma LH, FSH and prolactin secretion have been studied in rats at preovulatory periods (18th hour of diestrus). It has been found that administration of ethanol in preovulatory periods decreased the number of ovules per rat (p less than 0.001), the number of ovulating rats and LH levels (p less than 0.001). These effects were accompanied by an increase in prolactin concentration (0.05 greater than p greater than 0.02), which was followed by a diffuse luteinization in the ovarian tissue. These results showed that ethanol had an effect of central depression in preovulatory periods. These effects could be mediated through the hypothalamic releasing factors. Under previous serotonin depletion with p-chlorophenylalanine (PCPA: 300 mg/kg), ethanol caused similar effects on LH and FSH levels as compared with the control group with PCPA. However, prolactin concentration was not increased. These results showed that serotoninergic neurons could be mediated in changes caused by ethanol on prolactin secretion, but do not affect directly in changes caused on LH and FSH secretion.     

Environmental and social determinants of sexual function in the male lesser mouse lemur (Microcebus murinus).

Environmental factors that regulate the sexual activity of male lesser mouse lemurs have been studied experimentally with more than 60 captive animals over an 8-year period. In this nocturnal Malagasy prosimian, variation in day length is the primary factor controlling seasonal sexual activity. Plasma testosterone concentrations were low (= 9 ng/ml) during short days and reached 60 ng/ml during long days (> 12-hour day). This cyclic pattern persists unchanged when artificial photoperiodic rhythms are applied and is not altered by ageing. The timing of puberty is also regulated by photoperiodic changes. Nevertheless, the sexual activity of the male lesser mouse lemur can be dramatically modified by the social environment. In heterosexual groups, behavioural and physiological components of sexual activity are depressed in all males except the dominant one, whose aggressive interactions are always successful. Intermale sexual inhibition was shown to be mediated by chemical cues present in the urine of dominant or isolated males but not in urine of subordinate individuals. The inhibitory signals possess lipophilic properties and are not contingent on the gonadal activity of the urine donor but are linked to adrenocortical activity. By contrast, chemical signals stimulating the reproductive function of all males are found in the urine of females, the presence of which is required for the establishment of clear dominance among grouped males. Endocrine mechanisms underlying intermale sexual inhibition by chemical cues were analysed. Variations in prolactin strongly suggest that olfaction interacts with the photoperiodic regulation of reproductive function, leading to changes in the sensitivity of the negative feedback effect of testosterone on gonadotrophin secretion. Inhibitory or stimulatory effects of chemical signals are discussed in the context of their functional significance for wild populations.     

Development of the inhibitory guanine nucleotide-binding regulatory protein in the rat testis

The functional development of the inhibitory guanine nucleotide-binding regulatory protein (Gi) and anti-diuretic hormone (ADH) activity was investigated in rat testes. Adult (90-day-old), adolescent (40-day-old), prepubertal (23-day-old), and fetal (20.5 days of gestation) testis cells were cultured with 100 ng/ml pertussis toxin for 24 h. The cells were then cultured with human chorionic gonadotropin (hCG), the ADH agonist arginine vasotocin (AVT), or a combination of the two. Testis cells from rats 23, 40, and 90 days of age that were incubated with hCG increased testosterone production when compared with controls. Preincubation of the cells from postnatal rats with pertussis toxin significantly increased hCG-stimulated testosterone secretion when compared to cells preincubated in medium only at all three ages. AVT suppressed hCG-stimulated testosterone secretion, but this suppression was partially reversed in cells from all postnatal ages preincubated with pertussis toxin. Fetal testis cells showed no response to preincubation with pertussis toxin, even when levels were increased to 400 ng/ml or when pertussis toxin treatment was continued throughout the culture period. AVT also had no effect on fetal testis cells. These results indicate that the Gi protein and AVT are not functional in fetal testes but are active from prepubertal stages of development through maturity.     

Sexual hormones terminate in the rat: the significantly enhanced catecholaminergic/serotoninergic tone in the brain characteristic to the post-weaning period

The amount of dopamine released from the striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus and serotonin from the raphe, was significantly higher in four and five weeks old rats than in three month old ones, proving that the catecholaminergic/serotoninergic activity enhancer (CAE/SAE) regulation works unrestrained during developmental longevity and is restricted thereafter. As the dampening of the CAE/SAE regulation (end to the second month of age) coincided temporally with the appearance of sexual hormones, we castrated three weeks old male and female rats and measured at the end of the third month of their life the release of catecholamines and serotonin from selected discrete brain regions. The amount of catecholamines and serotonin released from the neurons was significantly higher in castrated than in untreated or sham operated rats, signalting that sexual hormones inhibit the CAE/SAE regulation in the brain. We therefore treated male and female rats s.c. with oil (0.1 ml/rat), testosterone, (0.1 mg/rat), estrone (0.01 mg/rat) and progesterone (0.5 mg/rat), respectively, and measured their effect on the CAE/SAE regulation. Twenty-four hours after a single injection with the hormones, the release of noradrenaline, dopamine and serotonin was significantly inhibited in the testosterone or estrone treated rats, but remained unchanged after progesteron treatment. In rats treated with a single hormone injection, testosterone in the male and estrone in the female was the significantly more effective inhibitor. Remarkably, the reverse order of potency was found in rats treated with daily hormone injections for 7 or 14 days. After two-week treatment with the hormones estrone was in the male and testosterone in the female the significantly more potent inhibitor of the CAE/SAE regulation. The data indicate that sexual hormones terminate the hyperactive phase of adolescence by dampening the impulse propagation mediated release of catecholamines and serotonin in the brain.     

Bromoergocryptine decreases serum prolactin and delays sexual maturation in male golden hamsters

The role of prolactin during sexual maturation in male golden hamsters was studied. Controls (n = 23) received vehicle and treated animals (n = 23) received 500 micrograms 2-bromo-alpha-ergocryptine (CB154) daily from 10 days of age until 4 or 5 wk of age. Serum prolactin in prepubertal male hamsters was reduced to a nondetectable level by treatment with the dopamine agonist CB154. Flank gland diameter, body weight, testicular and total accessory sex organ weights, and serum testosterone were all significantly lower (P less than 0.05) in the CB154-treated animals. In addition, seminiferous tubule area, seminiferous tubule luminal and cellular areas, and number of late spermatids per tubule cross-section were significantly reduced (P less than 0.01) in CB154-treated prepubertal males. Thus, the absence of prolactin retarded sexual maturation in male golden hamsters. These data suggest, that prolactin enhances testosterone production during the process of sexual maturation and supports the development of androgen-dependent tissues.     

The pubertal-related decline in cellular proliferation and neurogenesis in the dentate gyrus of male rats is independent of the pubertal rise in gonadal hormones

Pubertal development is marked by significant decreases in cellular proliferation and neurogenesis in the dentate gyrus of the hippocampal formation. Although it is unclear what mediates these developmental changes in the dentate gyrus, gonadal hormones have been implicated in modulating many neurobiological processes during puberty and various parameters of neurogenesis in adulthood. Thus, it is possible that the gradual and sustained increase in gonadal hormones experienced during puberty plays a role in these changes in neurogenesis. In this experiments, we first quantified cellular proliferation and neurogenesis using 5-bromo-2'-deoxyuridine (BrdU) and doublecortin (DCX) immunohistochemistry, respectively, in the dentate gyrus of prepubertal (30 d), midpubertal (45 d), and adult (90 d) male rats. We found the decline in BrdU and DCX cell numbers throughout these ages was coincident with increases in their plasma testosterone levels. We next tested whether exposure to the pubertal rise in gonadal hormones was necessary for this decrease in hippocampal neurogenesis to occur. Thus, we examined cellular proliferation and neurogenesis in intact 30 day (prepubertal) and 60-day-old (late-pubertal) rats, as well as 60-day-old rats that had previously been gonadectomized or sham-gonadectomized at 30 days of age. Although we again found the expected decline in BrdU and DCX cell numbers between 30 and 60 days of age in the intact groups, there were no differences among the 60-day-old animals, regardless of gonadal status. These data indicate that the pubertal-related decline in hippocampal cellular proliferation and neurogenesis is independent of the pubertal change in gonadal hormones.     

A developmental study of the gonadotropin-releasing hormone neuronal system during sexual maturation in the male Djungarian hamster.

The number, morphology, and distribution of gonadotropin-releasing hormone cell bodies were studied in the brain of the male Djungarian hamster during sexual maturation. Males were reared in long days (16L:8D) and were killed at 15, 25, or 40 days of age, before (n = 5), during (n = 4), or after puberty (n = 4), respectively. Brain sections (60 microns) from the rostral olfactory tubercle to the medial basal hypothalamus were processed for GnRH immunocytochemistry. Unipolar and bipolar neurons were immunolabeled for GnRH; both subtypes had smooth cell contours. Analysis of every section from the olfactory tubercle to the arcuate nucleus indicated that at all ages more than 75% of all GnRH-immunoreactive cell bodies were distributed in the diagonal band of Broca, medial preoptic area, lateral preoptic area, and lateral hypothalamic area. GnRH-positive somata were also found in other brain regions, but in each of these areas they represented less than 6% of the total GnRH neuron number. In peripubertal 25-day-old males, during the rapid phase of testes growth, the number of unipolar, but not bipolar, GnRH-labeled cells nearly doubled in the diagonal band of Broca compared to soma numbers in this location in prepubertal 15-day-old males. The same number of unipolar GnRH-stained somata were found in this region in 40-day-old as in 25-day-old hamsters. In the medial preoptic area, a similar doubling of unipolar neuron numbers was observed at 25 days, but by 40 days the number of unipolar immunostained GnRH cells was secondarily reduced to a level comparable to that at 15 days.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modulation by neonatal thymectomy of the reproductive axis in male and female rats during development

The effects of neonatal thymectomy, at 3 days of age, on parameters of the reproductive axis were examined in male and female Sprague-Dawley rats. Gonadal and accessory sex tissue (male: epididymis, seminal vesicle, and ventral prostate; female: uterus) weights as well as anterior pituitary, spleen, and adrenal weights were determined in the thymectomized and sham-thymectomized animals at 20, 30, 40, 50, 60, and 90 days of age. Plasma gonadotropin concentrations as well as pituitary content of the gonadotropins and prolactin were assessed at each of these time intervals. No significant difference in gonad and accessory sex tissue weights was detected in thymectomized versus sham-operated controls at each of these times. Adrenal weights were increased in thymectomized animals compared with controls at 50 days of age and older in male rats and at 90 days in females. Spleen weights were decreased in the thymectomized males at 50 and 60 days of age. Thymectomy did not affect the spleen weight of females. Plasma concentrations of gonadotropins were unaffected in thymectomized males but were altered in females during the pre- and peripubertal period (Days 20-40). Vaginal opening, however, occurred at the same time in the thymectomized and control females. Pituitary gonadotropin and prolactin content were unaffected by thymectomy of the females, except at 90 days when pituitary luteinizing hormone (LH) content was lower in thymectomized than in control animals. LH and prolactin content were significantly reduced in the males at 60 and 90 days of age. These results demonstrate that there are sexual differences in the effects of thymectomy on parameters of the reproductive axis.(ABSTRACT TRUNCATED AT 250 WORDS)