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PubMed1995

The effect of prenatal exposure to the phytoestrogen genistein on sexual differentiation in rats.

Exposure to naturally occurring estrogens during critical periods of development can alter morphologic and physiologic markers of sexual differentiation. The current experiment characterizes the effects of in utero treatment with genistein, an isoflavonoid phytoestrogen, on birth weight, anogenital distance (AGD) at birth. GnRH stimulated luteinizing hormone (LH) secretion, volume of the sexually dimorphic nucleus in the preoptic area of the hypothalamus (SDN-POA), puberty onset, and vaginal cyclicity. Pregnant Charles River CD rats were injected sc daily on gestation day 16-20 with either 25,000 micrograms genistein (G25), 5,000 micrograms genistein (G5), 5 micrograms diethylstillbestrol (DES), 50 micrograms estradiol benzoate (E), or corn oil alone for controls. Birth weights and anogenital distance was taken and exposed progeny were subsequently used in two experiments. In Experiment 1 intra-atrial catheters were placed in adult castrated rats, GnRH was given iv, serial blood samples were drawn and sera were assayed for LH by radioimmunoassay (RIA). Brains obtained by subsequent decapitation were saved for histology. In Experiment 2, females were monitored for timing of vaginal opening as a marker of puberty onset, and vaginal smears were taken to monitor cyclicity. G25-treated females and DES- and E-treated animals of both sexes had decreased weights at birth compared with controls. G5- and E-treated animals of both sexes and DES males had smaller AGD than controls. No significant differences in pituitary responsiveness to GnRH were found among treatment groups. There was a nonsignificant decrease in SDN-POA volume in G5-treated females while DES- and E-treated females had increased SDN-POA volume compared with controls. G5-treated females had delayed puberty onset, and DES-treated females had atypical vaginal cycles in comparison with controls. The results confirm that prenatal exposure to estrogens in the environment can influence sexual differentiation. Our previous experiments have demonstrated that castrate female rats exposed as neonates to genistein have decreased pituitary responsiveness to GnRH challenge and enlarged SDN-POA volume in comparison with controls. Prenatal genistein at these dosages did not significantly alter these markers. However, genistein did mimic other estrogens' effects on AGD and birth weight and had a unique influence on puberty onset. Not only are genistein's effects different from other estrogens, but dosage and timing of exposure during development appear to be important factors in genistein's ability to modify these end points.

Animals↗
PubMed2002

The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.

Recently we reported that atrazine (ATR), a chlorotriazine herbicide, alters the onset of puberty in male Wistar rats. In this study, we examined the same reproductive parameters in the developing male rat following a similar exposure to the primary, chlorinated metabolites of atrazine. Intact male Wistar rats were gavaged from postnatal day (PND) 23 through PND 53 and several reproductive endpoints were examined. The doses selected were the molar equivalents to atrazine in our previous work. Deethylatrazine (DEA), deisopropyl-atrazine (DIA), and diaminochlorotriazine (DACT) were administered by gavage at doses equivalent to the atrazine equimolar doses (AED) of 6.25, 12.5, 25, 50, 100, or 200 mg/kg. Preputial separation (PPS) was significantly delayed by DEA at 25, 100, and 200 AED, by DIA at 25, 100, and 200 AED, and by DACT at 12.5 through 200 AED. When the males were killed on PND 53, DEA (100 and 200 AED), DIA (50 through 200 AED), and DACT (200 AED) treatments caused a significant reduction in ventral prostate weight, while only the highest doses of DIA and DEA resulted in a significant decrease in lateral prostate weight. Seminal vesicle weight was reduced by DEA (25, 100, and 200 AED), DIA (100 and 200 AED), and 100 and 200 AED of DACT. Epididymal weights were reduced in the DEA (200 AED), DIA (200 AED), and DACT (100 and 200 AED) treatment groups. Serum testosterone was reduced only in the males receiving the 2 highest doses of DIA. Serum estrone was increased in the 2 highest doses of the DACT group, while serum estradiol was not different in any group. No differences were observed in any of the thyroid measures. In summary, the metabolites of ATR delay puberty in a manner similar to that observed in the previous study testing atrazine. These data also suggest that the 3 chlorinated metabolites are similar to ATR, by affecting the CNS control of the pituitary/gonadal axis and subsequent development of the reproductive tract.

Animals↗
PubMed2007

Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor.

BACKGROUND: A single family has been described in which obesity results from a mutation in the leptin-receptor gene (LEPR), but the prevalence of such mutations in severe, early-onset obesity has not been systematically examined. METHODS: We sequenced LEPR in 300 subjects with hyperphagia and severe early-onset obesity, including 90 probands from consanguineous families, and investigated the extent to which mutations cosegregated with obesity and affected receptor function. We evaluated metabolic, endocrine, and immune function in probands and affected relatives. RESULTS: Of the 300 subjects, 8 (3%) had nonsense or missense LEPR mutations--7 were homozygotes, and 1 was a compound heterozygote. All missense mutations resulted in impaired receptor signaling. Affected subjects were characterized by hyperphagia, severe obesity, alterations in immune function, and delayed puberty due to hypogonadotropic hypogonadism. Serum leptin levels were within the range predicted by the elevated fat mass in these subjects. Their clinical features were less severe than those of subjects with congenital leptin deficiency. CONCLUSIONS: The prevalence of pathogenic LEPR mutations in a cohort of subjects with severe, early-onset obesity was 3%. Circulating levels of leptin were not disproportionately elevated, suggesting that serum leptin cannot be used as a marker for leptin-receptor deficiency. Congenital leptin-receptor deficiency should be considered in the differential diagnosis in any child with hyperphagia and severe obesity in the absence of developmental delay or dysmorphism.

Adult↗
PubMed1978

The anti-reproductive pharmacology of LH-RH and agonistic analogues.

LH-RH and three particular ("super") analogues were evaluated for agonistic (ovulation-induction and short-term uterotrophic properties) and postcoital contraceptive activity in rodents. Additionally, LH-RH and/or a representative analogue (D-Ala6-des Gly10-Pro9-LH-RH ethylamide) were tested for postcoital contraceptive/vaginal smear/return to fertility effects, precoital contraceptive activity, and effects on puberty in the immature female. All compounds induced ovulation and uterotrophic effects and terminated pregnancy when administered either pre- or post-implantation. LH-RH and the representative analogue, while terminating pregnancy postcoitally, produced an associated break in the characteristic leucocytic vaginal smear of pregnancy to one of cornification by day 12; at this time mating and insemination were reestablished and all rats carried to normal term. Precoitally, LH-RH administered to nembutalized (but not to unblocked) rats produced a 50% reduction in the pregnancy rate and a 38% decrease in the number of viable pups delivered. In immature rats, the representative analogue delayed puberty (i.e. vaginal canalization) and retarded the growth of the ovaries, uteri, and anterior pituitary gland. The collective data strongly support the concept that LH-RH and agonistic derivatives, in spite of their putative pro-fertility classification, are characteristically antifertility by nature. Since the latter effect appears to be the paradoxically dominant one, it is suggested that LH-RH agonism is synonymous with contraception. Furthermore, such peptides may represent a new potential approach to fertility control.

Animals↗
PubMed1987

Absence of an increase in gonad-independent drive to pulsatile luteinizing hormone secretion during photoperiod-induced puberty.

This study was conducted to determine if photoperiod can influence the pattern of luteinizing hormone (LH) secretion in the absence of the ovaries in the developing female sheep. Lambs were raised in a photoperiod sequence (short, long, short days) known to induce puberty between 30 and 35 wk of age, or in a photoperiod (only short days) that prevents puberty during the first year. Their ovaries were removed at 10 wk of age, and the detailed pattern of LH was assessed (samples at 12-min intervals for 4 h) each 3- to 5-wk period between 9 and 45 wk of age. Rapid LH pulses (40- to 50-min interpulse interval) were evident within a few weeks after ovariectomy in both groups of females. Those exposed to the artificial photoperiod sequence that induces normal sexual maturity did not increase their pulse frequency further during the pubertal period. Moreover, their LH pulse frequencies were not greater than those in agonadal females exposed to the photoperiod that delays puberty. These findings indicate that photoperiodic induction of puberty in the sheep does not require steroid-independent modulation of pulsatile LH secretion.

Animals↗
PubMed1982

The reproductive endocrine system in cystic fibrosis: 2. Changes in gonadotrophins and sex steroids following LHRH.

Hypothalamic-pituitary-gonadal function was assessed in forty-seven patients with cystic fibrosis (CF) by the 3-hr infusion of 100 microgram of synthetic gonadotrophin-releasing factor. LHRH and the results compared with a group of children being evaluated for short stature and delayed puberty ('controls'). Levels of gonadotrophins and sex steroids were measured prior to and during the infusion. In prepubertal boys, LH and FSH release evoked by LHRH was significantly greater (P less than 0.001) in 'control' subjects than in CF patients. In pubertal boys, LH and FSH release was also greater in 'controls' than in CF, though to a lesser degree (P less than 0.05). In pubertal girls, responses to LHRH were comparable for LH and slightly greater (P less than 0.05) in 'controls' for FSH. In the earliest pubertal groups of both sexes (male-Tanner genitalia stage 2; females-Tanner breast stage 2), LH secretion was similar in patients with CF and 'control' subjects. Significant increments of testosterone and oestradiol in pubertal CF patients do not occur until 6 h after the LHRH infusion begins, in contrast to a rise at 3 h in 'control' subjects. These data suggest that prepubertal boys with CF, who are the most impaired in height, weight and skeletal maturation, also have measurable abnormalities of LHRH-releasable gonadotrophin secretion. Despite continued impaired weight growth, pubertal patients do attain essentially normal gonadotrophin secretory responses to LHRH administration and are similar to subjects with constitutional delayed adolescent development in reproductive endocrine physiology.

Adolescent↗
PubMed2004

[Puberty and growth in children and adolescents with neuro fibromatosis type 1].

BACKGROUND: This study evaluates anthropometric and pubertal development parameters in children and adolescents with sporadic and familial occurrence of neurofibromatosis type 1 (NF-1). METHODS: The study involved 23 patients (15 boys, 8 girls) with sporadic (n=12) and familial NF-1(7 affected mothers and 4 fathers), with average age of 12 years (range 5-20 years). All patients answered to a standard questionnaire including family and personal data and, following, they underwent systematized physical examination, with special attention to anthropometric data, dermatologic and pubertal stage according to Tanner's criteria evaluation. RESULTS: Short stature was detected in a 17 year-old patient, 148.5cm height, with score Z of -4.16 and being the even outside of the family conduit. Three male patients had head circumference above of + 2DP from on average for the age. It was not found no case of precocious or delayed puberty. CONCLUSIONS: In our study, do not we find significant alterations regarding the stature and pubertal development.

Adolescent↗
PubMed1997

Problems in diagnosis of IBD in children.

Children and adolescents with inflammatory bowel disease (IBD) present unique challenges to physicians and all health-care providers. The most important aspect is that children are not small adults. They are characterized by a highly dynamic state of growth and physical change as well as a constant alteration in psychological status. It will not be difficult to recognize IBD, even in children, when it presents with classical symptoms such as bloody diarrhoea, abdominal pain and weight loss. However, some children will present with abdominal pain and depression. Not infrequently these children are diagnosed as being depressed and are seen and treated by psychologists and psychiatrists for different periods of time. In addition, several children will be initially diagnosed as having a bacterial gastroenteritis with a proven positive faecal culture. It seems to be the triggering event in these children, and if adequate therapy fails, colonoscopy is indicated. Recently, Beattie et al. showed that in children seen for chronic abdominal pain simple routine blood tests including full blood count and erythrocyte sedimentation rate are almost always abnormal in children with IBD. But most importantly, growth retardation is common in children with IBD and is more often found in Crohn's disease (CD) than in ulcerative colitis (UC). Faltering growth is a sign of a catabolic situation. Therefore, it is essential to follow the growth of children at the beginning and during treatment of IBD. Growth retardation can be the first symptom of IBD and is often already present before other symptoms of IBD become apparent. Rarely, extra-intestinal manifestations, particularly arthritis, can be the first and sometimes only initial symptom for months to years in children with IBD. About 2% of all patients with IBD present before the age of 10 years, but 30% present between the age of 10 and 19 years. A significant proportion of young patients with IBD will develop the disease just prior to or during puberty. Adolescent growth is characterized by rapid accumulation of lean body mass and any inflammatory disease occurring at this time is likely to have a major impact on nutritional status and growth. This rapid growth requires an appropriate increase in nutritional substrates and failure to achieve catch-up growth may ultimately lead to poor cumulative growth over time. Most of the growth retardation is seen in children with CD, approximately 30%. However, also in UC 15% will show a reduction in growth. The higher percentage in CD could be due to the disease itself or to the relative subtlety of the intestinal manifestations of CD, mainly abdominal pain and general malaise. Not only growth, but also delayed puberty, is a sign of an ongoing disease that most likely needs more intensive treatment. It has been shown that the severity of disease activity plays a more important role in the occurrence of growth retardation than steroid treatment. Therefore in paediatrics it is important to state that growth retardation during medical treatment equals undertreatment. In contrast to adults, the potential benefit of nutritional therapy should be seriously considered in addition to aggressive medical therapy including steroids and other immunosuppressive agents such as azathioprine. The most convincing evidence that malnutrition is primarily responsible for growth failure is based on depletion studies. The malnutrition itself is caused by ongoing inflammation and loss of appetite. Recommendations for nutritional therapy include an increase in energy and protein intake to 150% of recommended daily allowances for height and age. Some studies have shown the benefit of nocturnal nasogastric infusion as supplements of daily intake. Importantly, nutritional support has been shown to be as effective as steroids in achieving remission of disease in children. Furthermore, no significant differences have been shown in studies using elemental versus polymeric diets.

Adolescent↗
PubMed1999

Gestational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) severely alters reproductive function of female hamster offspring.

Low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), administered as a single dose to the dam during gestation, alter development of the fetal rodent reproductive system. In male rat and hamster offspring, dosing with TCDD during gestation reduces epididymal and ejaculated sperm counts and delays puberty. In female rats, in utero TCDD-exposure results in reduced ovarian weight and fecundity, and induces cleft phallus and a persistent thread of tissue across the vaginal orifice. Here, we demonstrate that 2-microgram TCDD/kg, administered as a single oral dose prior to sexual differentiation, alters reproductive function in female hamster offspring, a species relatively resistant to the lethal effects of TCDD. In the current study, pregnant hamsters (P0 generation) were dosed orally with vehicle (corn oil) or 2 micrograms TCDD/kg on gestational day (GD) 11.5. P0 maternal viability, body weight, fertility, and F1 litter size did not differ between control and treated groups. In the F1 generation, body weights were permanently reduced by about 30%, vaginal opening was delayed (p < 0.0001), and vaginal estrous cycles were altered by TCDD treatment. In contrast, most treated female offspring displayed regular 4-day behavioral estrous cycles, indicating that in utero TCDD treatment did not markedly disrupt hypothalamic-pituitary-gonadal hormonal cyclicity. Although both control and TCDD-treated F1 females mated successfully with a control male (estrous cyclicity was abolished by mating), 20% of the F1 treated females did not become not pregnant (no implants). In addition, 38% of pregnant F1 females from the TCDD group died near-term, and the numbers of implants in pregnant animals (treated 5.1 versus 11.3) and pups born live (2.7 treated vs. 8.7 control) were reduced by TCDD-treatment. In the F2, survival through weaning was drastically reduced (15% treated vs. 78% for control) by TCDD treatment of P0 dams. F1 female hamster offspring exposed in utero to TCDD displayed external urogenital malformations, with most females having complete clefting of the phallus, an effect previously reported in the rat. Unlike rats exposed to TCDD (0.2-1.0 microgram/kg) on GD 15 or GD 8, hamster offspring did not display vaginal threads. These results demonstrate that in utero administration of TCDD adversely affects growth, reproductive function, and anatomy in female hamster offspring given a dosage level nearly four orders of magnitude below the dosage level toxic to the adult animal. Adverse effects of TCDD persisted through two generations (F1 and F2), even though the F1 was only indirectly exposed during gestation and lactation.

Animals↗
PubMed1986

Social mediation of puberty: an adaptive female strategy?

Females of two hamster species with contrasting degrees of gregariousness were tested for social influences on the timing of sexual maturation. When female dwarf hamsters (Phodopus sungorus campbelli), a gregarious species, were housed with an adult male at weaning, they began estrous cycles significantly earlier than when they were housed alone or with their family. Females housed with one or two female siblings at weaning matured significantly later than did all other females. Once mature, females housed with familiar males conceived later than did females housed with unfamiliar males. Rearing conditions also affected body weight; those housed with female siblings grew more slowly and attained a lower weight at 8 weeks of age than did females in all other groups. In contrast, when weanling female golden hamsters (Mesocricetus auratus), a solitary species, were housed with either an adult male, two female siblings, or alone, they did not differ in their rate of sexual maturation or growth. It is suggested that the degree to which social factors can accelerate or delay puberty is an adaptive characteristic and may be correlated with the degree of gregariousness of a species.

Animals↗
PubMed1999

Pubertal growth of the short normal girl.

OBJECTIVES: To determine the timing, magnitude and duration of the pubertal spurt for short normal and average height girls, to compare these with Tanner's standard and to investigate predictors of pubertal growth. METHODS: The growth of 46 short normal and 55 control girls, identified at school entry, was monitored throughout puberty. Height and weight were measured at 6-month intervals from which body mass index (BMI) was derived. Annual velocities were calculated and used to estimate the age and magnitude of peak height velocity (PHV). Age of menarche was recorded to the nearest month. Parents provided information on the child's medical and social history. RESULTS: The mean age at PHV, the magnitude of PHV and age at menarche were similar for both groups and close to Tanner's 50th centile values. Pre-pubertal BMI predicted age at menarche for short and control girls, accounting for 17% of the variance. There was a tendency for early maturing girls of average stature to have greater PHV. However, this relationship was not observed in short girls, nor did any other variable, genetic or environmental, predict the timing or magnitude of their pubertal spurt. CONCLUSIONS: Delayed puberty in short normal girls is unlikely and their growth during puberty is comparable to girls of average height. The pubertal variables measured remain close to Tanner's original standards for both groups, suggesting the lack of a secular trend towards earlier puberty in girls. The onset of menstruation is influenced by pre-pubertal BMI. However, the clinician should be aware that short normal girls have normal pubertal growth and that no genetic or environmental variable can predict the timing or magnitude of their growth spurt.

Adolescent↗
PubMed2005

Testicular development of Zebu bulls after chronic treatment with a gonadotropin-releasing hormone agonist.

The objective was to compare testis characteristics of Zebu bulls treated with the GnRH agonist, deslorelin, at different times and for different durations during their development. An additional objective was to determine the usefulness of a stain for the transcription factor GATA-binding protein 4 (GATA-4) as a specific marker for Sertoli cell nuclei in cattle. Bulls (54) were allocated to nine groups (n = 6) and received s.c. deslorelin implants as follows: G1 = from birth to 3 mo of age; G2 = from 3 to 6 mo; G3 = from 6 to 9 mo; G4 = from 9 to 12 mo; G5 = from birth to 15 mo; G6 = from 3 to 15 mo; G7 = from 6 to 15 mo; G8 = from 12 to 15 mo; and G9 (control) = no implant. Bulls were castrated at 19 mo of age. Paraffin sections (10 microm) were subjected to quantitative morphometry and GATA-4 immunohistochemistry. At castration, all bulls in the control group (6/6) had attained puberty (scrotal circumference > or = 28 cm), whereas a smaller proportion (P < 0.05) had reached puberty in G2 (2/5) and G6 (1/6). Bulls in G2 and G6 also had a lesser (P < 0.05) testis weight compared with the control group. Total volume of seminiferous epithelium and total daily sperm production in G2 and G6 were only half that observed in the control group. Spermatids were observed in less than 50% of seminiferous tubules in G2, G6, and G7 compared with 82% in the control group (P < 0.05). Staining for GATA-4 was specific for and abundant in the Sertoli cell nucleus in both pre- and postpubertal bulls, and no other cell nucleus inside the seminiferous tubule was positive for GATA-4. Total number of Sertoli cells was not affected by treatment (P = 0.45), but nuclear volume was smaller in G2 and G6 (P < 0.05) compared with the control group. In conclusion, treatment of Zebu bulls with deslorelin had no apparent beneficial effect on testis development and delayed puberty when treatment was initiated at 3 mo of age. Staining for GATA-4 was a useful method for identifying and quantifying Sertoli cell nuclei in both pre- and postpubertal bulls.

Animals↗
PubMed1992

Behavioral selection of odor cues by young female mice affects age of puberty.

Female house mice were reared from weaning at 21 days of age until first vaginal estrus in 40 1 aquaria in which they were given a choice of exposing themselves to bedding placed on opposite halves of the aquarium floor and sprayed with water or urine containing puberty-influencing chemosignals. In Experimental 1, mice housed with only male urine cues sprayed on the bedding matured significantly earlier and mice housed with only grouped female urine sprayed on the bedding matured significantly later than control mice where water was sprayed on the bedding for both halves of the aquarium. In Experiment 2, there were no significant differences in mean ages at vaginal introitus or first estrus for females reared with choices between (a) bedding sprayed with male urine versus bedding sprayed with water, (b) bedding sprayed with urine from grouped females versus bedding sprayed with water, (c) bedding sprayed with male urine versus bedding sprayed with urine from grouped females, or (d) the control condition where both sides of the aquarium contained bedding sprayed with water. Analysis of continuous video tapes of the locations of the females for Experiment 2 revealed that females chose initially to spend more time on the half of the floor with bedding that delayed puberty relative to the other side, but shifted their preference toward a more puberty-enhancing signal at about the time of first estrus. Female house mice appear to be able to exert some behavioral control over their own sexual maturation.

Age Factors↗
PubMed2006

Normal values for the scrotal circumference in rams of gotlandic breed.

Selection of fertile sires is crucial for profitable lamb production. Males with larger testes tend to sire daughters that reach puberty at an earlier age and ovulate more ova during each oestrus period. Measurement of the scrotal circumference (SC) is thus an essential part of the breeding soundness evaluation. Testicular size varies with breed, age and time of the year. No SC values or recommendations for minimal values have been established in any of the Scandinavian domestic sheep breeds. Data were recorded of the SC, age and weight in 245 ram lambs and 27 mature rams of the Gotlandic breed, which is the breed that constitutes about 50% of the Swedish sheep population. For the ram lambs, the overall mean SC was 28.9 (+/-1.9) cm at an average age of 170 (+/-9) days and mean weight of 53.5 (+/-7.0) kg, and the mean SC varied between 27.1 and 29.6 cm depending on age and weight. For mature rams (17-54 month old), the mean SC was 32.4(+/-2) cm. To provide a practical tool for exclusion of rams with sub-optimal reproductive capacity (abnormal testes or those with small testes because of delayed puberty) a threshold value was established based on the average SC minus 2 SD. The calculated minimal SC is 26 cm for ram lambs >5.5 months of age with a body weight of >50 kg. For mature rams, minimum SC is 28 cm regardless of weight and age.

Age Factors↗
PubMed1999

Mutations and polymorphisms in gonadotropin genes.

Mutations in gonadotropin genes are extremely rare. Only one case of inactivating human luteinizing hormone (LH) beta mutation exists in the literature, a male with absence of Leydig cells, lack of spontaneous puberty and infertility. A total of four cases of inactivating mutation of the follicle-stimulating hormone beta (FSHbeta) gene (two female and two male) are known. The phenotype of the women was primary amenorrhea and absence of follicular maturation, the men were azoospermic. In addition, a common genetic variant (v) of LH was recently discovered. It is caused by two point mutations in the LH beta-subunit gene, resulting in amino acid alterations: Trp8 --> Arg and Ile15 --> Thr. In addition, the latter change introduces an extra glycosylation signal for oligosaccharide attachment to Asn13. The v-LHbeta allele has a carrier frequency ranging from 0 to > 50% in various populations. The variant LH molecule has increased intrinsic bioactivity in vitro, but decreased circulatory half-life in vivo, and the v-LHbeta promoter is about 50% more active in cell line transfections than that of wild-type (wt) LH. These differences in LH synthesis and action in individuals homo- or heterozygous for the v-LH allele are reflected by altered disposition to pathologies of pituitary-gonadal function, such as delayed puberty, polycystic ovarian syndrome and infertility.

Female↗
PubMed1998

Epidermal growth factor tyrosine kinase receptors and the neuroendocrine control of mammalian puberty.

In recent years evidence has begun to accumulate indicating that the central control of mammalian puberty requires not only changes in transsynaptic communication, but also the participation of glial cells. Neurons and astrocytes control the pubertal process by regulating the secretory activity of those neurons that produce luteinizing hormone-releasing hormone (LHRH), the neuropeptide that governs sexual development. LHRH, in turn, directs sexual development by stimulating the secretion of pituitary gonadotropins. Astrocytes affect LHRH neuronal function via cell-cell signaling mechanisms involving several growth factors acting via receptors endowed with tyrosine kinase activity. We have identified two members of the epidermal growth factor/transforming growth factor alpha (EGF/TGFalpha) family and their respective receptors as key players in the glial-neuronal interactive process that regulates LHRH secretion. Our results indicate that TGFalpha and its distant congener neuregulin (NRG) are produced in hypothalamic astrocytes and stimulate LHRH release indirectly via activation of their respective receptors, located--surprisingly--not on LHRH neurons, but on astrocytes. Activation of EGF receptors by TGFalpha, and/or the erbB2/erbB4 receptor complex by NRG, leads to glial release of prostaglandin (PG) E2, which then acts directly on LHRH neurons to stimulate LHRH release. That a central blockade of TGFalpha or NRG action delays puberty, and focal overexpression of TGFalpha advances it, leads to the conclusion that both TGFalpha and NRG are physiological components of the central mechanism controlling the initiation of female puberty.

Animals↗
PubMed2004

Chronic somatostatin treatment affects pituitary gonadotrophs, ovaries and onset of puberty in rats.

The effects of chronic somatostatin (SRIH-14) treatment on the pituitary gonadotrophs (FSH and LH cells) and ovaries of female Wistar rats were examined. Females were given 20 microg/100 g b.w. twice per day from the immature (23rd day) till the adult period of life (71st day). The onset of puberty was determined by daily examination for vaginal opening. The peroxidase-antiperoxidase immunocytochemical procedure was used to study the gonadotrophs. Changes in the number per unit area (mm2), cell volume and volume densities of LH- and FSH-immunoreactive cells were evaluated by morphometry and stereology. Ovaries were analysed by simple point counting of follicles and corpora lutea (CL). Follicles were divided by size according to the classification of Gaytán and Osman. The mitotic indexes of granulosa and theca cells in the follicles were estimated at all stages of folliculogenesis. The number, volume and the volume density of FSH- and LH-immunoreactive cells decreased after chronic SRIH-14 treatment, particularly the latter. In the ovary, SRIH-14 treatment decreased the number of healthy follicles at all phases of folliculogenesis, lowered the mitotic indexes of granulosa and theca cells but increased the number of atretic follicles. Healthy CL were fewer in number, while regressive CL were increased. Vaginal opening occurred at a later age in treated females. It can be concluded that chronic SRIH-14 treatment markedly inhibited LH cells and to a lesser extent FSH cells. In the ovary SRIH-14 inhibited folliculogenesis, enhanced atretic processes and lowered proliferative activity of granulosa and theca cells. It also delayed puberty onset.

Animals↗
PubMed1998

Nitro(w)-arginine methyl ester treatment delayed the onset of puberty in female rats.

It is well documented that nitric oxide (NO) stimulates LHRH, LH and GH release. Present experiments were carried out to analyse whether the blockade of NO generation can affect body growth and puberty onset in female rats. Prepubertal female rats were treated with L-nitro(w) arginine methyl ester (NAME), a blocker of nitric oxide synthase, from day 25 to first estrous (400 or 800 mg/L in drinking water). We measured body growth, age and body weight at vaginal opening and first estrous, and the ovarian and uteri weights and serum LH and FSH concentrations the day of first estrous. Females treated with NAME showed a normal body growth pattern and a delayed puberty. Serum LH concentrations were increased in groups treated with NAME. This stimulatory effect was also observed in 30 and 90 day-old females decapitated 60 min after NAME administration (40 mg/Kg i.p.). We conclude that blockade of NO generation delays puberty in female rats by mechanism(s) other than its effects on LH release.

Animals↗