Telencephalic connections of the sexually dimorphic area of the gerbil hypothalamus that influence male sexual behavior.

The sexually dimorphic area (SDA) of the gerbil hypothalamus is essential for mating in male gerbils. To determine if it affects mating through its connections with the ventral part of the lateral septal nucleus (LSv), the caudal part of the medial bed nucleus of the stria terminalis (caudal BSTm), or the medial amygdala-amygdalohippocampal area (MA-AHi), these connections were severed. Unilateral cell-body lesions were made in the SDA and in the contralateral LSv, caudal BSTm, or MA-AHi. Controls received the same lesions ipsilaterally. Other gerbils received lesions in the caudal BSTm and contra- or ipsilateral MA-AHi. Only contralateral lesions of the SDA and caudal BSTm severely impaired mating. Because contralateral lesions of the SDA and MA-AHi, or BSTm and MA-AHi, did not mimic this effect, the BSTm neurons that are needed for male sexual behavior through their connections with the SDA do not simply relay information to or from the MA-AHi.

Sexually dimorphic cell groups in the medial preoptic area that are essential for male sex behavior and the neural pathways needed for their effects.

The research summarized here shows that the two major cell groups of the sexually dimorphic area (SDA) of the gerbil hypothalamus are essential for male sex behavior. Bilateral cell-body lesions of either the medial or lateral SDA virtually eliminate mating in sexually experienced male gerbils given exogenous testosterone. Similar deficits occur when the SDA is bilaterally disconnected from the retrorubral field (RRF) as a result of unilateral cell-body lesions in the SDA and contralateral RRF. The A8 cells of the RRF do not account for this effect. Bilaterally disconnecting the SDA from the caudomedial part of the bed nucleus of the stria terminalis (caudal BSTm) also eliminates sexual activity. Disconnecting the SDA from the medial amygdala does not mimic this effect. Neither does disconnecting the medial amygdala from the caudal BSTm. Thus, caudal BSTm neurons that are essential for mating via connections with the SDA do not simply relay information from the medial amygdala.

Embryonic differentiation of sexual dimorphism in vasotocin and mesotocin levels in chickens.

Chicken embryos of both sexes were injected on the tenth day of incubation with either estradiol benzoate (EB), aromatase inhibitor [1,4,6-androstatrien-3, 17-dione (ATD)], antiestrogen [tamoxifen (TAM)], antiandrogen [flutamide (FLU)], or the oil vehicle as control (C). At adulthood, at the age of 26 weeks, 10 chickens of each sex were killed and the amounts of immunoreactive arginine vasotocin (AVT) and mesotocin (MT) in the anterior hypothalamus (AHA), posterior hypothalamus (PHA), neurohypophysis (NHP), and pineal gland (PNL) were determined. Control hens had significantly more AVT in PNL and less MT in AHA and NHP than the corresponding roosters. This sexual dimorphism was affected by the embryonic treatments; TAM increased AVT in AHA of cockerels but not of hens. In both sexes, TAM and FLU increased AVT content in NYP. In males, but not in females, ATD also increased AVT content in the NHP. TAM and FLU administration to the female embryo reduced PNL AVT to the amount present in normal males. None of the treatments effected AHA MT in hens, while in cockerels TAM increased it. In females, TAM and FLU significantly increased NHP MT to the level of C males. In roosters, ATD, TAM, and FLU increased NHP MT further. In hens, but not roosters, FLU reduced MT in PNL. These results indicate that embryonic differentiation of the MT and AVT systems is affected by gonadal steroids in chickens.

Sexual differentiation of copulatory behaviour in the male chick requires gonadal steroids.

1. Embryonic injections of 0.3 mg/egg of tamoxifen (TAM), 0.2 mg/egg CI-628 (both antioestrogens), 0.5 mg/egg (ATD (aromatisation inhibitor), or antibodies to oestradiol (E), all suppressed male copulatory activity (MCA) in young male chicks. 2. Embryonic injections with either flutamide (F, androgen antagonist) or high dose of antibodies to testosterone (T) only slightly suppressed MCA. 3. TAM had no effect on embryonic plasma LH levels, 24 and 48 h after injection. 4. It seems that at the embryonic stage oestradiol is required for the normal differentiation of MCA.

The effects of embryonic treatments with gonadal hormones on sexually dimorphic behavior of chicks.

In order to study the role of sex steroids in the differentiation of chick behavior, two groups of experiments were carried out. The first part of the study documented sexual dimorphisms in three behavioral measures in chicks: open-field activity, flocking response, and masculine sexual behavior activated by testosterone (crowing, waltzing, and mating attempts). In the second part, possible organizing influences on these sexually dimorphic behaviors were examined. Male and female embryos were injected with estradiol benzoate (EB) or testosterone propionate (TP). Treatment of males with EB or TP demasculinized all three behaviors. None of the steroid treatments had any effect on the behavior of the females. Plasma testosterone levels of the chicks were not affected by any of these treatments, either before or after testosterone activation. Comb weight was reduced by treatment of male embryos with EB and increased by TP in female embryos, which suggests different mechanism for the development of somatic and behavioral characteristics. The results suggest that exogenous T or E given embryonically can exert similar effects on both sexual behavior and nonreproductive activity of chicks.

Effects of sex and gonadal steroids on arginine vasotocin and mesotocin in the pineal gland and neurohypophysis of White Leghorn fowls.

1. Pineal and neurohypophysial arginine vasotocin (AVT) and mesotocin (MT) were measured in White Leghorn hens, cockerels and castrated males treated with either testosterone propionate (TP) or oestradiol benzoate (EB) (n = 10/group). The lighting regimen was 14 h light: 10 h dark, supplied by natural diffused sunlight and incandescent bulbs. 2. Both AVT and MT were detected in the pineal gland of all the chickens. 3. There was no significant effect of either sex or treatments on pineal MT. 4. Females had about 4 times more pineal AVT than males, regardless of their treatment. There was no effect of the treatments on pineal AVT in the males. 5. No sexual difference in neurohypophysial AVT was detected, but the neurohypophysis of the castrated males treated with EB contained less AVT than the neurohypophysis of the intact males. 6. Intact males had about twice as much MT in the neurohypophysis as females. Castrated males treated with either TP or EB had similar concentrations of neurohypophysial MT, which were lower than that of the intact males, but higher than that of the females.

Embryonic sex steroids affect mating behavior and plasma LH in adult chickens.

Chicken embryos of both sexes were treated with either antiestrogen (tamoxifen = T), antiandrogen (flutamide = F), aromatization inhibitor (ATD = A), estradiol (E), or oil (control = C). Before puberty, some males of each group were castrated. At puberty, birds were tested under the following regimes: castrated males injected daily with testosterone propionate (CAS + TP) or estradiol benzoate (CAS + EB), intact males (M-INT), intact females (F-INT), and females injected daily with TP (F-TP). In the M-INT and CAS + TP males, E treatment suppressed masculine mating behavior. The embryonic treatments with T, F, and A demasculinized only the frequency of copulations. None of the antihormone treatments caused any masculinization of the sexual activity in the F-TP birds. Untreated males had higher plasma LH than females. The embryonic treatment with E reduced (feminized) the LH levels in CAS + EB birds. This effect was less pronounced in M-INT birds. The results suggest that in chickens, estradiol plays a role in the masculinization of copulatory behavior potential in the developing male embryo. High embryonic estradiol reduces the potential for displaying male sexual behavior at puberty. Feminization of LH secretion requires a high level of estradiol in both embryonic and adult life.

Fertile semen from 9-week-old chicks treated with tamoxifen.

White Leghorn male chicks were injected with 1 mg/kg BW of tamoxifen (an anti-estrogen) on alternating days between 2 and 9 wk of age. This treatment increased testes weight and induced semen production in response to the abdominal massage procedure. Insemination of laying hens with this semen resulted in hatching of live chicks from their eggs.

Effect of embryonic treatment with estradiol benzoate on the aggressive behavior of cockerels.

The purpose of this work was to study the effects of early embryonic treatment with estradiol on the aggressive behavior of cockerels, following castration and administration of testosterone or estradiol in adult life. Embryonal estradiol eliminated adult aggressive behavior. However estradiol activation after castration resulted in typical male cock fighting.

Testosterone and adiposity in the chicken: the effect of breed and sex.

The leaning role, previously suggested for testosterone in chickens, was tested in males and females of fatty and lean breeds. The breeds used were the White Leghorn (WL), of which the male is very lean, and the White Giant (WG) and the White Cornish X White Rock (WCWR), in which both sexes accumulate fat. Castration of WL males induced adiposity and replacement therapy with testosterone propionate (TP) reduced the fat to normal. However, in males of the fatty breeds, neither castration nor TP administration had any effect on adiposity. Similarly, long-term supplementation of a high dose of TP had no effect on the level of adiposity in females of both the heavy and the light breeds. Thus, the leaning effect found for testosterone in the WL male is not a general phenomenon in chickens but rather a specific response of the WL male.

Induction of precocious development of reproductive function in cockerels by tamoxifen administration.

To examine the effects of tamoxifen, a known estrogen antagonist in the chicken, two groups of cockerels were injected every other day from hatching until 7 weeks of age with 1 and 10 mg tamoxifen/kg body weight (BW), respectively. A third group was injected with 1 mg tamoxifen/kg BW every 3 days from 5 to 10 weeks of age. All groups treated with tamoxifen had increased testes weight, but BW and pituitary weights did not differ from controls. In contrast to controls, seminiferous epithelium of testes from treated cockerels showed spermatogenesis up to the spermatid elongation stage. We suggest that the antiestrogen effect of tamoxifen increased circulating LH, which stimulated testes growth and precocious spermatogenesis.