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Castration fantasies and assertiveness in father-absent males.

In a previous report (Shill 1981), father-absence was linked to insecurity in core male gender identity in a nonclinical sample of college males. The present paper describes further aspects of the experimental use of projective techniques, based on psychoanalytic theory and clinical discussions, to assess the effect of father-absence on male personality development. Castration fantasies and sense of competence in the mastery of external reality as an index of masculine self-representation were coded from the projective test responses of 103 father-present and 28 father-absent college males. When given a choice of castrating figure at the human or animal level, all subjects identified the human mother rather than the father as the more frightening castrating figure. Father-absent subjects, however, identified the animal mother as the more frightening castrating figure, compared to the animal father, more frequently than the father-present subjects, suggesting a denial and displacement of castration fear toward the human mother onto the animal substitute. The father-absent subjects also evidence significantly less sense of mastery, suggesting less self-assertiveness and sense of competence than the father-present controls. The importance of identification with the father as the basis for a masculine ego style and of father absence as a developmental interference affecting the appropriate management of aggression in males is discussed.

Adult↗

Neonatal castration of male and female rats affects hypothalamic and pituitary estrogen nuclear and progestin cytosol receptors.

We compared the effects of neonatal or adult castration (7 days) and 2 or 7 days of estrogen treatment on the concentrations of estradiol cystolic (ERc) and nuclear (ERn), and progestin cytosolic receptors (PRc) in the hypothalamus, amygdala and pituitaries of adult rats. Two days of estradiol (E2) treatment greatly increased ERn levels, but no further concentration changes occurred by Day 7 in any of the tissues. Long- and short-term castrated males and females had comparable ERn concentrations on Day 2 versus Day 7. Tissue ERn levels were significantly lower in short-term males compared to short-term females or neonatally castrated males and females. In a second study, ERn levels were compared in E2-treated short-term castrated males and females on Day 2. A sex difference was observed, with females having greater ERn levels in most areas. Estrogen significantly increased PRc levels in pituitary (PIT) and hypothalamus, and these levels were comparable in Day 2 and Day 7 animals. Thus, the ability of estrogen to induce PRc synthesis is somewhat refractory in long-term castrated rats.

Aging↗

Maintenance of androgen-, glucocorticoid- or estrogen-responsive growth in shionogi carcinoma 115 subline sustained in castrated mice with high dose of estrogen for 30 generations (3 years).

Shionogi carcinoma 115 (SC115), an androgen-dependent mouse mammary tumor, rapidly loses its androgen responsiveness after androgen withdrawal. The growth of this tumor can also be stimulated by high doses of estrogen or glucocorticoid. In the present study, the maintenance of hormone-responsive growth of SC115 tumors with a high dose of estrogen was examined in castrated male mice using an SC115 subline obtained by serial transplantations of SC115 tumors in estrogen-treated castrated mice for 3 years (30 generations) (subline E2). Seed tumors from both SC115 and subline E2 could rapidly grow in castrated mice given daily injections of testosterone propionate (TP), 17 beta-estradiol (E2), or dexamethasone (Dex) (100 micrograms/mouse/day) but not in those given vehicle alone. Although SC115 and subline-E2 tumors grown with TP or Dex showed temporary regression after steroid withdrawal, the tumors grown with E2 did not show such temporary regression. The TP-, E2-, or Dex-induced growth of subline-E2 tumors was almost the same as that of the original SC115 tumors. However, responsiveness to androgen, estrogen or glucocorticoid of both tumors disappeared within one passage in steroid-depleted castrated mice. The present findings demonstrate that the loss of responsiveness to androgen as well as to high doses of estrogen or glucocorticoid of SC115 tumors can be prevented in castrated mice not only with androgen but also with high doses of estrogen.

Animals↗

Effects of castration and testosterone on Fel dI production by sebaceous glands of male cats: I--Immunological assessment.

Fel dI is produced by salivary and sebaceous glands. Hormonal control of sebum production is clearly established. The influence of cat castration and supplementary treatment with testosterone on the production of sebum and Fel dI in cat skin have been researched in this study. On day 1, 12 male cats were anaesthetized and three skin areas carefully shaven. Then the level of lipids on skin surface was measured by means of a photometric method. Finally, the three areas of skin were washed with 5ml of distilled water through a plastic cylinder. Fel dI collected in the washes was measured with a two-site monoclonal antibody based ELISA. On day 2, six cats were castrated, the other six were used as a control group. Two and 4 weeks later, the levels of lipids and Fel dI in skin washes were measured again in all cats. On day 30, the six castrated cats were injected intramuscularly with prolonged-action testosterone. Two weeks later, quantification of lipids and Fel dI in all animals was repeated. Sebum and Fel dI levels decreased in all castrated animals. Injecting the castrated cats with testosterone led to a significant increase in sebum and Fel dI production. Our findings indicate that Fel dI production is influenced by the production of hormones.

Allergens↗

Absence of adrenal influence on ovarian graft activity in male rats castrated at birth.

1. An investigation was made to see whether the presence of the adrenal gland was necessary for cyclical activity of ovarian transplants in adult male rats which had been castrated at birth.2. Rats were castrated on the day of birth or at 6-8 weeks of age and when 3 months old were adrenalectomized and had a transplant of immature ovary placed in the anterior chamber of one eye. Control animals were subjected to the same procedure apart from adrenalectomy.3. Transplants in rats castrated at birth were observed to undergo full cyclical activity, with follicular rupture and the formation of corpora lutea. Transplants in rats castrated at 6-8 weeks of age did not cycle and corpora lutea were not formed.4. Adrenalectomy did not influence the behaviour of the ovarian transplants.5. It is concluded that the presence of the adrenal gland was not necessary to support cyclical activity in ovarian tissue transplants in male rats castrated at birth.

Adrenal Glands↗

Effects of castration on nitric oxide-mediated relaxations in male rat corpus cavernosum smooth muscle.

BACKGROUND: The effects of castration on nitric oxide- mediated relaxations and nitric oxide synthase activity in male rat corpus cavernosum smooth muscles. METHODS: Eight-week-old male rats were assigned to two groups: control (sham operated) and castrated animals. After 8 weeks, corpus cavernosum smooth muscle strips were mounted in an organ bath for isometric tension recordings. Electrical field stimulation (EFS) was applied to the strips precontracted with 30 microM phenylephrine. The microdialysis probe was inserted into the strip, and Krebs-Henseleit solution was perfused into the probe. The dialysate during EFS and cholinergic stimulation was collected, and the amount of NO(-)(2)/NO(-)(3) (NOx) released in the dialysate was measured by the Greiss method. Sodium nitroprusside and carbachol were cumulatively added to the strips precontracted with 30 microM phenylephrine. RESULTS: EFS caused frequency-dependent relaxations and NOx releases in the strips. Pretreatment with N(omega)-nitro-L-arginine (100 microM) and tetrodotoxin (1 microM) completely inhibited relaxations and NOx releases. The maximum relaxation in the castration group was significantly greater than that in the control group. The release of NOx was significantly greater in the castration group than in the control group. Sodium nitroprusside relaxed the tissues in both groups similarly. Carbachol failed either to relax the tissue or to increase the amount of NOx production in the tissue. CONCLUSION: The present data suggest that castration enhances nitric oxide synthase activity and nitric oxide-mediated relaxations in the male rat corpus cavernosum.

Animals↗

Effects of coincubation of the pituitary and hypothalamus of intact and castrate male rats and the influence of LH-RH on pituitary 5 alpha-reductase activity1,2.

Pituitary 5 alpha-reductase activity in intact male rats increases after the pituitary is incubated with the hypothalamus. Incubating the pituitary of castrate rats with the hypothalamus of intact rats relatively inhibits pituitary 5alpha-reductase activity. Coincubation of the pituitary and hypothalamus of castrate rats, or the pituitary of intact with the hypothalamus of castrate males, does not elicit changes in pituitary 5alpha-reductase activity. Different amounts of LH-RH in the incubation medium can modify 5alpha-reductase activity, i.e., activate it in the intact pituitary and inhibit it in the castrate pituitary. Hypothalamus from intact rats, which according to SHIN et al. [1974] is 'rich' in LH-RH, induces changes in pituitary 5alpha-reductase activity. The LH-RH-'poor' hypothalamus of castrate rats does not cause changes in this enzyme activity. The results suggest that there is a very close relationship between LH-RH and 5alpha-reductase activity in the pituitary.

Animals↗

Comparison of the effect of castration on the development of postural and non-postural muscles of mice.

The effect of castration on the development of muscle mass of postural and non-postural muscles was studied in 18 male mice (9 castrated, 9 uncastrated). Results obtained indicated that the castrated males grew faster and were bigger in body size and weight at maturity than the intact males. The bigger body size of castrated males was not due to larger muscle mass but was probably due to increased subcutaneous fat deposition. Atrophy of muscles usually observed following castration was significantly greater in the non-postural (biceps brachii) muscle of the forelimb as compared to the postural (triceps brachii) muscle of the forelimb. Conversely, the amount of reduction in muscle mass was similar in both postural (soleus) and non-postural (tibialis cranialis) muscles of the hindlimb.

Animals↗

Gonadotropin secretion in cryptorchid and castrate rams and the acute effects of exogenous steroid treatment.

Gonadotropin secretion in cryptorchid and castrate rams and the acutve been determined. Rams made cryptorchid at 6 weeks of age had increased serum levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) when determined at 9 months of age. These levels approached those of the castrate animal; and yet serum levels of testosterone (T) were unchanged. Even though mean serum LH concentrations were elevated sixfold to eightfold over those of intact ram levels, a temporal relationship between this hormone and T was observed similar to that reported in the intact ram. Intramuscular injections of dihydrotestosterone had no effect on circulating levels of LH or FSH in either cryptorchid or castrate rams, whereas T effectively reduced these gonadotropins in castrate but not in cryptorchid rams. Only estradiol-17beta (E2) was effective in both cryptorchid and castrate rams. Estradiol was a potent inhibitor of LH secretion; however, its effect on FSH levels was less dramatic. This suggests that testicular products other than E2 may be important in the regulation of FSH production and/or release. Importantly, the inhibition of LH secretion lasted less than 12 h; whereas, the negative effects of E2 on FSH secretion lasted 72 to 144 h. In conclusion, results from this study show that T is not the single factor responsible for regulation of LH and FSH secretion in male sheep. Estradiol may be an important regulator of gonadotropin secretion, but 5alpha-reduction plays no apparent role in this process.

Animals↗

Examination of prolactin and pituitary-adrenal axis components as intervening variables in the adrenalectomy-induced inhibition of gonadotropin response to castration.

Adrenalectomy performed at the same time as, or 12 h after, castration delays the postcastration rise in LH and FSH for at least 12 h. We tested three mechanisms previously advanced as possible mediators in this suppression: 1) blocking PRL in castrate-adrenalectomized males with bromoergocryptine did not restore the normal postcastration rise in serum LH and FSH, eliminating high PRL levels as a cause of this gonadotropin suppression; 2) exogenous ACTH given at the time of orchidectomy did not inhibit either gonadotropin, eliminating high peripheral ACTH as an agent of adrenalectomy-induced suppression of LH and FSH; and 3) intestinal traction performed at the same time as orchidectomy suppressed the secretion of LH and FSH to the same degree as adrenalectomy, ruling out the lack of any adrenal factor as a means by which adrenalectomy blocked gonadotropin secretion. Our data suggest that the adrenalectomy-induced suppression of LH is due to a neurally mediated stress response probably resulting in suppression of GnRH secretion. In other treatment groups, we implanted cortisol before surgery to test the effect of ACTH suppression on LH and FSH secretion in castrate-adrenalectomized animals. A striking divergence between LH and FSH was seen in response to cortisol treatment. Cortisol suppressed LH, but not FSH, in castrate animals, and restored postcastration FSH, but not LH, secretion 12 h after combined castration-adrenalectomy. This divergence between LH and FSH secretion suggests that the effect of adrenalectomy on the two gonadotropins might result from different mechanisms. It is also possible that the differential effect of cortisol on LH and FSH secretion is not relevant to the effect of adrenalectomy on the postcastration secretion of these gonadotropins. These data add to the evidence, however, that LH and FSH are regulated by different mechanisms under many experimental conditions, including stress and elevated corticoid levels.

Adrenalectomy↗

Does prolactin modify testosterone feedback in the hamster? Pituitary grafts alter the ability of testosterone to suppress luteinizing hormone and follicle-stimulating hormone release in castrated male hamsters.

Adult male golden hamsters maintained in a long photoperiod (14 h of light and 10 h of darkness) or in a short photoperiod (5 h of light and 19 h of darkness for 7 weeks) were castrated and either given one anterior pituitary transplant under the kidney capsule or sham-operated. Additional animals were castrated and grafted or sham-grafted at the time of transfer to the short photoperiod. Starting 2 weeks after castration, all animals were injected three times a week with 20 micrograms testosterone propionate (TP). After 3 weeks, the dose of TP was increased to 80 micrograms and, after an additional 2 weeks, to 320 micrograms per injection. Blood samples were collected 2 weeks after castration and 1 day after the last injection of 20, 80, and 320 micrograms TP. Short photoperiod reduced and pituitary grafts increased plasma PRL levels. Plasma testosterone levels were related to the dose of injected TP, but were not influenced by photoperiod or pituitary transplants. Before the onset of TP injections, plasma LH and FSH levels in grafted and sham-grafted hamsters did not differ. In each of the three photoperiod conditions, injections of TP were consistently less effective in suppressing plasma gonadotropin levels in pituitary-grafted animals than in sham-grafted controls. These results indicate that PRL modulates the effects of exogenous testosterone on LH and FSH release in adult castrated male golden hamsters, this effect of PRL is due to reducing the sensitivity of the hypothalamic-pituitary system to feedback inhibition by testosterone, and suppression of pituitary PRL release in short photoperiod may be partially responsible for the concomitant increase in the sensitivity of LH and FSH release to inhibition by testosterone.

Animals↗

Effects of photoperiod, castration, and gonadotropin-releasing hormone (GnRH) on the number of GnRH receptors in male golden hamsters.

Maintenance of male golden hamsters on short photoperiod leads to testicular regression due to pineal gland-mediated inhibition of the hypothalamo-hypophyseal reproductive system. This study clarifies the dynamics of the action of GnRH at the pituitary level after short photoperiod-induced gonadal regression. In Exp 1, adult male golden hamsters were injected with BSA or varying doses of exogenous GnRH every 8 h for 3 days. There was no effect on the number of GnRH receptors, indicating that GnRH does not increase the number of its own receptors in hamsters as it does in rats. In Exp II, adult male golden hamsters were placed on a 14-h light, 10-h dark lighting schedule (LD 14:10) or LD 6:18. Nine weeks later, half of the animals on each photoperiod were castrated, and 10 weeks after initiation of the experiment, intact and castrated hamsters were decapitated. Intact hamsters on LD 6:18 had the expected reduction in serum LH levels and testicular weight compared to intact animals on LD 14:10. There was a postcastration rise in serum LH in both groups, but the increase was attenuated in the animals on short photoperiod. Castration of animals on LD 14:10 resulted in an increased number of GnRH receptors per pituitary, but this increase was at least partly due to an increase in pituitary weight. Intact animals on LD 6:18 had fewer pituitary GnRH receptors than intact hamsters on LD 14:10, but this decrease was not due solely to a decrease in pituitary weight. These results indicate that maintenance on short photoperiod results in a decreased number of pituitary GnRH receptors. In Exp III, intact animals on LD 6:18 responded to 1 microgram GnRH, sc, with an increment in LH secretion similar to that in intact animals on LD 14:10. Castration of animals on long photoperiod increased the LH response to GnRH, but castration of hamsters on short photoperiod did not. In conclusion, a reduced number of pituitary GnRH receptors may be involved in the testicular regression associated with short photoperiod in male golden hamsters.

Animals↗

Effects of castration and chronic steroid treatments on hypothalamic gonadotropin-releasing hormone content and pituitary gonadotropins in male wild-type and estrogen receptor-alpha knockout mice.

Testicular androgens are integral components of the hormonal feedback loops that regulate circulating levels of LHbeta and FSH. The sites of feedback include hypothalamic areas regulating GnRH neurons and pituitary gonadotropes. To better define the roles of androgen receptor (AR), estrogen receptor-alpha (ERalpha), and estrogen receptor-beta (ERbeta) in mediating feedback effects of sex steroids on reproductive neuroendocrine function, we have determined the effects of castration and steroid replacement therapy on hypothalamic GnRH content, pituitary LHbeta and FSHbeta messenger RNA (mRNA) levels, and serum gonadotropins in male wild-type (WT) and estrogen receptor-alpha knockout (ERKO) mice. Hypothalami from intact WT and ERKO males contained similar amounts of GnRH, whereas castration significantly reduced GnRH contents in both genotypes. Replacement therapy with estradiol (E2), testosterone (T), or dihydrotestosterone (DHT) restored hypothalamic GnRH content in castrated (CAST) WT mice; only the androgens were effective in CAST ERKOs. Analyses of pituitary function revealed that LHbeta mRNA and serum LHbeta levels in intact ERKOs were 2-fold higher than those in intact WT males. Castration increased levels of LHbeta mRNA (1.5- to 2-fold) and serum LHbeta (4- to 5-fold) in both genotypes. Both E2 and T treatments significantly suppressed LHbeta mRNA and serum LH levels in CAST WT males. However, E2 was completely ineffective, and T was only partially effective in suppressing these two indexes in the CAST ERKO males. DHT treatments stimulated a 50% increase in LHbeta mRNA and serum LH levels in WT males, whereas serum LH was significantly suppressed in DHT-treated ERKO males. Although the pituitaries from intact ERKO males contained similar amounts of FSHbeta mRNA, serum FSH levels were 20% higher than those in the intact WT males. Castration increased FSHbeta mRNA levels only in WT males, but significantly increased serum FSH levels in both genotypes. Both E2 and T treatments significantly suppressed serum FSH in CAST WT males, whereas only E2 suppressed FSHbeta mRNA. DHT treatments of CAST WT mice stimulated a small increase in serum FSH, but failed to alter FSHbeta mRNA levels. None of the steroid treatments exerted any significant effect on FSHbeta mRNA or serum FSH levels in CAST ERKOs. These data suggest that hypothalamic GnRH contents can be maintained solely through AR signaling pathways. However, normal regulation of gonadotrope function requires aromatization of T and activation of ERalpha signaling pathways in the gonadotrope. In addition, serum FSH levels in male ERKOs appear to be regulated largely by nonsteroidal testicular factors such as inhibin. Finally, these data suggest that hypothalamic ERbeta may not be involved in mediating the negative feedback effects of T on serum LH and FSH in male mice.

Animals↗

Changes of serum gonadotropin concentrations in fetal and neonatal rat following castration.

Changes of serum concentrations of LH were measured in fetal and neonatal rats following castration. Intact fetal and neonatal male rats showed low levels of serum LH concentration. Though serum LH levels of male rats casterated on the 20th day of gestation did not significantly increase by the 22nd day of fetal age, serum levels of neonatal male rats increased 2-to 3-fold 3 days following castration at all ages studied. The increase was greater in 4-day-old male rats than in 1-day-old males. The increase of serum LH after castration was also found in 4-day-old male rats castrated on the 20th day of gestation. In contrast, serum levels of 1-day-old neonatal female rats did not increase 3-days after castration. These observations suggest sex differences in maturation of the gonadal-hypophyseal feedback mechanism.

Animals↗

Effect of alloxan diabetes on kidney growth in intact and castrated mice.

The mouse kidney is particularly responsive to the withdrawal or administration of androgens. The absence of endogenous androgens after castration led to decreased RNA synthesis and subsequent decrease in weight of the kidney. The induction of diabetes in 21 days castrated mice restored kidney weight. In intact mice made diabetic by iv injection of alloxan there was a increase in kidney weight. This increase was accompanied by a proportional increase in RNA. In mice hypertrophy was found to be the major factor in renal growth. When castration and diabetes were combined kidney weight did not fall as in the case of castration only but increased even above the kidney weight of intact animals. There was a parallel rise in RNA content of the kidney. Castration does not inhibit the renotropic activity of alloxan diabetes in mice. Renal growth in alloxan diabetes is quite independent of the presence of androgens.

Androgens↗

Effects of short-term treatment with testosterone on the secretion of FSH and LH in castrated golden hamsters exposed to short days.

Castrated hamsters which were transferred from long (14L:10D) to short (9L:15D) days and received testosterone-filled capsules for 1 week after transfer failed to show a significant suppression in the plasma levels of FSH and LH after capsule removal. In contrast, gonadotrophin concentrations were suppressed in hamsters in which the long-day castration response had been blocked with exogenous testosterone. After castration on long days and exposure to 10 weeks of short days pituitary gland weight and gonadotrophin content, as well as plasma FSH titres, were higher in control animals than in those that had received testosterone implants for 7 weeks of short days. The results suggest that failure of castrated hamsters to respond to the suppressive effects of short days reflects castration-induced changes in hypothalamo-pituitary physiology rather than a neuroendocrine mechanism by which photoperiod modulates gonadotrophin secretion.

Animals↗

Influence of castration on development of the thymus in neonatal male rats.

The influence of castration on the development of the thymus in neonatal rats was studied to elucidate when after birth the thymus comes under inhibitory regulation by the testis in rats. The relative and absolute weights of the thymus were measured five days after castration these cases. No excessive changes in the weights of the thymus with castration were observed by 31 days after birth. Significant changes in the thymus appeared in the relative weight at 36-day-castration. The absolute weight of the thymus was also significantly increased after 41-day-castration. These findings suggest that in rats the inhibitory regulation of the thymus by testis development does not appear before at least 31 days of age.

Aging↗

Changes in hypophysio-ovarian endocrinological function of post-menopausal and castrated women.

The serum levels of estradiol, progesterone, LH and FSH were determined by radioimmunoassay in post-menopausal and castrated women and the data obtained at the same periods after menopause and castration were compared. The serum levels of estradiol and progesterone in post-menopausal women within 1 year after menopause were higher than those of castrated women. The result suggested that ovarian function was indeed depressed in the post-menopausal women but was still preserved for 1 to 2 years after menopause. In the post-menopausal women, the levels of serum LH and FSH rose gradually to reach a peak at 1 to 3 years after menopause, when the production of ovarian sex steroid hormones presumably ceased. On the contrary, the serum LH and FSH levels of castrated women began to decrease gradually 4 to 9 years after castration. It is highly suggestive from these findings that a negative feedback mechanism is elicited by ageing.

Aging↗