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PubMed2003

Effect of repeated ketoprofen administration during surgical castration of bulls on cortisol, immunological function, feed intake, growth, and behavior.

To determine the effect of repeated ketoprofen (K) administration to surgically castrated bulls on cortisol, acute-phase proteins, immune function, feed intake, growth and behavior, 50 Holstein x Friesian bulls (11 mo old; 300 +/- 3.3 kg) were assigned to one of five treatments: 1) untreated control (C); 2) surgical castration at 0 min (S); 3) S following an i.v. injection of 3 mg/kg of BW of K at -20 min (SK1); 4) S following 1.5 mg/kg of BW of K at -20 and 0 min (SK2); or 5) S following 1.5 mg/kg of BW of K at -20 and 0 min and 3 mg/kg of BW of K at 24 h (SK3). Castration acutely increased plasma cortisol concentrations in S- and K-treated animals compared with C, with no differences in peak and interval to peak cortisol responses among the castration groups. Overall, the integrated cortisol response was greater (P < 0.05) in the castrates than in C, whereas K treatments decreased (P < 0.05) this response compared with S alone, with no differences between K treatments. Plasma haptoglobin and fibrinogen concentrations were increased (P < 0.05) on d 3 in the castration groups compared with C as the result of tissue trauma induced by castration, whereas SK1 and SK2 had lower (P < 0.05) haptoglobin concentrations than S animals. On d 1, concanavalin A-induced interferon-gamma production was suppressed (P < 0.05) in S and SK3 compared with C, SK1, and SK2 animals. Overall from d 1 to 33, DMI were lower (P < 0.05) in S, SK1, and SK3 than in C animals. From d -1 to 35, ADG were lower (P < 0.05) in S, SK2, and SK3 compared with C animals. A higher (P < 0.05) incidence of standing postures and lower incidence of lying postures was observed in S compared with C during the first 6 h after treatment. However, the higher (P = 0.02) incidence of abnormal standing activities observed for S was reversed (P < 0.05) by the K treatments. In conclusion, surgical castration increased plasma cortisol and acute-phase proteins and decreased immune function, feed intake, and growth rate. Ketoprofen effectively reduced the cortisol response to castration, but there was no advantage in treating with two split doses of K (1.5 mg/kg of BW per dose). A repeated K dose 24 h after treatment (3 mg/kg of BW) had no influence on changes in acute-phase proteins and immune response. Systemic analgesia with K is an effective method for alleviating acute inflammatory stress associated with castration.

Acute-Phase Proteins↗
PubMed2006

Hormonal profiles, behavioral responses, and short-term growth performance after castration of pigs at three, six, nine, or twelve days of age.

The objective of this study was to determine the effects of castration on short-term growth performance, hormone profiles, and behavior in pigs at 3, 6, 9, or 12 d of age. Ninety intact male pigs were assigned randomly to a treatment age by litter [3, 6, 9, or 12 d of age; n = 9 to 13 pigs per treatment (age) group]. Pigs within a single litter were then assigned to noncastrated (NC) or castrated (CAS) treatment groups according to BW. Pigs were nonsurgically fitted with jugular catheters, and blood samples were drawn immediately before castration (0 h) and at 0.5, 1, 1.5, 2, 24, and 48 h after castration. Body weights were obtained when pigs were catheterized and again at 24 and 48 h after castration. Serum samples were analyzed for cortisol, porcine corticosteroid-binding globulin, and dehydroepiandrosterone sulfate (DHEA-S). No differences were detected in initial BW of pigs, and there was no overall treatment effect on growth performance of pigs at 24 or 48 h posttreatment. A time x treatment interaction was detected (P < 0.01) for serum cortisol concentrations, such that cortisol was greater in CAS pigs than in NC pigs. No overall effect of age at castration was observed on cortisol concentrations. At 24 h after castration, serum cortisol concentrations returned to baseline in all treatment groups; however, at 48 h after castration, overall cortisol concentrations were elevated (P < 0.01) in the 6-, 9-, and 12-d-old pigs in both the CAS and NC groups compared with baseline concentrations. Total cortisol and porcine corticosteroid-binding globulin were used to calculate the free cortisol index (FCI). A time x treatment interaction was observed (P < 0.01) for FCI, such that FCI was greater in CAS males than in NC males. The FCI was also affected by age (P < 0.01). There was a time x treatment x age interaction (P < 0.01) for serum DHEA-S, such that DHEA-S concentrations decreased in CAS animals but increased in NC animals, and DHEA-S concentrations increased with age. During the first 2 h after castration, there was an overall age effect (P = 0.01) on the time that pigs spent standing, such that 3-d-old pigs stood more than 6-, 9-, or 12-d-old pigs. Treatment did not influence the time that pigs spent nursing, lying, standing, or sitting, although there was a trend (P = 0.08) for CAS pigs to be less active than NC pigs. These data indicate that castration is stressful regardless of age; however, the stress associated with handling seems to increase as pigs age.

Aging↗
PubMedDate not supplied

The antigonadotropic action of testosterone but not 7alpha-methyl-19-nortestosterone is attenuated through the 5alpha-reductase pathway in the castrated male rat pituitary gland.

The enzyme 5alpha-reductase plays a significant role in the prostate to amplify the action of testosterone (T) by converting it to a more potent androgen, dihydrotestosterone (DHT). The role of 5alpha-reductase in the testosterone feedback inhibition of gonadotropin secretion from the pituitary has not been elucidated. Therefore, we investigated the role of 5alpha-reductase on T action in in vitro and in vivo models. Castration has been reported to increase the 5alpha-reductase activity in pituitary glands. Hence, the effect of castration duration on the conversion of T to DHT by pituitary homogenates and the responsiveness of pituitary monolayer cell cultures to gonadotropin-releasing hormone (GnRH) challenge exposure were investigated. Incubation of [3H]-T with pituitary homogenates showed that the conversion of T to 5alpha-reduced metabolites was two- to threefold greater in pituitaries from rats who had been castrated for 14 days compared with those castrated for 1 day. In addition, the GnRH-stimulated release of LH from monolayer cell cultures of pituitaries from rats castrated for 1 day was twofold greater, whereas that from rats castrated for 2 weeks was six- to sevenfold greater compared with basal luteinizing hormone (LH) release. Hence we used rats castrated for 2 weeks to elucidate the role of 5alpha-reductase in T feedback inhibition. The inhibitory effects of the androgens T, 19-nortestosterone (19-NT), and 7alpha-methyl-19-nortestosterone (MENT) at 3 different concentrations (10(-9), 10(-7), and 10(-5) mol/L) on GnRH-stimulated LH release from monolayer cell cultures of pituitaries from rats castrated for 2 weeks were examined. All 3 androgens showed dose-dependent inhibition of LH release. MENT showed the greatest inhibition, followed by 19-NT and T. In the presence of finasteride (a 5alpha-reductase inhibitor), the inhibition of LH released by T and 19-NT were significantly greater. The inhibitory effect of MENT, which does not undergo 5alpha-reduction, was not altered by finasteride. In an in vivo study, rats castrated for 2 weeks received T with or without finasteride. There was a significantly greater suppression of serum LH in rats receiving T plus finasteride compared with those receiving T alone. These results suggested that 5alpha-reductase in the pituitary is not obligatory for the inhibitory action of T on gonadotropin secretion in the castrated rat. The action of MENT, a nonreducible androgen, on the pituitary is not affected by 5alpha-reductase.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed2001

Biomarker analysis demonstrates a hypoxic environment in the castrated rat ventral prostate gland.

Within the first 24 h after castration of an adult male rat, the vascular system of the ventral prostate gland undergoes a degenerative process that drastically reduces blood flow to the tissue. Since the vascular degeneration precedes the loss of the prostatic epithelium (by apoptosis), we have proposed that the onset of epithelial cell apoptosis in this tissue is caused by an ischemic/hypoxic environment resulting from the loss of blood flow. In order to further evaluate the extent to which ischemia/hypoxia might be a factor in apoptosis of the prostate epithelium after castration, we analyzed for biomarkers of cellular hypoxia in rat ventral prostates during the first 3 days following castration. Ventral prostate tissues removed from hypoxyprobe-1-treated adult male rats (uncastrated controls; surgically castrated for 24, 48 or 72 h, or sham-castrated for equivalent times) were directly analyzed for evidence of hypoxia by in situ immunohistochemical evaluation of hypoxyprobe-1 adduct formation in the prostate cells. Protein extracts from these tissues were also tested for expression of the 120 kDa hypoxia-inducible factor-1-alpha (HIF-1-alpha) protein as well as for expression of mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) proteins using a Western blot assay. The tyrosine phosphorylation status of the latter signaling molecules was also evaluated by Western blotting using anti-tyrosine phosphate antibodies. Our results showed that epithelial cells of the rat ventral prostate stained positively for hypoxyprobe-1 adducts at all times after castration, whereas cells in control tissues were unstained by this procedure. In addition, the prostatic expression of HIF-1-alpha protein was increased approximately 20-fold at 48 h after castration compared to control tissues. Finally, although prostatic MAPK and JNK protein expression was unaltered during the early period after castration, phosphorylation of the JUN kinase protein was significantly elevated, indicating that this stress-activated cellular signaling pathway becomes more active subsequent to castration. These results support our proposal that early castration-induced degeneration and constriction of the vascular system of the rat ventral prostate gland leads to reduced oxygenation of prostatic epithelial cells and the activation of hypoxic cellular signaling in these cells through upregulation of HIF-1-alpha expression and stimulation of the JUN kinase signaling pathway.

Animals↗
PubMed1991

Effect of estradiol implanted in the corticomedial amygdala on the sexual behavior of castrated male rats.

1. The purpose of the present investigation was to study the effect of beta-estradiol crystals implanted in the corticomedial area of the amygdaloid body on the sexual behavior of castrated male rats. 2. The animals were divided into the following groups: group I (N = 9), castrated rats; group II (N = 4), rats which had been castrated and stereotaxically implanted with cholesterol, both groups being used as controls; group III (N = 6), castrated rats with estradiol implants. Latency to the first anogenital exploration, latency to the first mount and mount frequency were determined during the pre-castration and post-castration phases and after the material had been implanted in groups II and III in 10-min observation sessions. 3. There was diminished sexual behavior of the animals in group I without spontaneous recurrence within the period observed. Group II animals, who had undergone implantation of cholesterol, an inert substance, maintained low levels of sexual behavior (post-castration 0.8 +/- 0.7 vs 0.0 +/- 0.0 and 0.5 +/- 0.5 on the 6th and 9th day after implantation, respectively). Group III animals presented a gradual increase in the number of mounts (from post-castration 1.2 +/- 0.5 to 6.5 +/- 2.7 and 4.1 +/- 1.0 on the 6th and 9th day after implantation, respectively) and a decrease of mount latency (from post-castration 431.2 +/- 55.9 to 226.1 +/- 119.6 and 51.0 +/- 28.9 on the 6th and 9th day after implantation, respectively) reaching pre-castration levels on the 6th and 9th day after beta-estradiol implantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1990

Treatment of R-3327 prostate tumors with a somatostatin analogue (somatuline) as adjuvant therapy following surgical castration.

This study addresses, in an animal tumor model, the clinical problem of "escape from castration inhibition." Somatuline (BIM-23014C), an octapeptide analogue of somatostatin with enhanced potency and longer duration of biological activity was administered as a therapeutic agent, over a period of 90 and 197 days, to male Copenhagen rats bearing syngeneic Dunning R-3327-H prostate tumors. Androgen sensitivity was confirmed by the response of tumors to castration and by the significant inhibition of tumor growth in intact animals by treatment with a luteinizing hormone-releasing hormone antagonist (BIM-21009). Inhibition of tumor growth resulting from castration persisted for 102 days, after which progressive regrowth occurred, indicating an escape from castration inhibition. When Somatuline treatment was initiated as an adjuvant therapy 5 days after castration, the rate of tumor regrowth during escape was significantly retarded. During the period of 197 days postcastration, tumors in the vehicle-treated, intact controls grew to an average diameter of 38.6 +/- 7.6 mm and tumors in vehicle-treated castrate controls grew to an average diameter of 23.3 +/- 4.1 mm (60% test/control). Treatment with the luteinizing hormone-releasing hormone antagonist induced no significant additional tumor inhibitory effects in castrated animals which developed tumors having an average diameter of 30.2 +/- 8.2 mm (78% test/control). Treatment of tumors in castrate animals with Somatuline, on the other hand, induced a significant (P less than 0.01) tumor-inhibitory effect that was greater than that produced by castration alone, developing an average tumor diameter of only 14.3 +/- 2.6 mm, (37% test/control). A growth inhibitory effect was also inducible in animals having tumors that had already escaped castration inhibition. The relative nontoxicity of a somatostatin analogue such as Somatuline suggests that chronic or maintenance therapy of slow-growing prostate cancers may be both feasible and acceptable in a clinical setting.

Animals↗
PubMed1983

Sexual behavior in response to testosterone in old long-term-castrated rhesus males.

The sexual behavior of 20-year-old long-term-castrated and intact male rhesus macaques (Macaca mulatta) was observed. In the first experiment we compared the sexual behavior of males tested in 1980 with their performance in 1970 (before castration and sham castration) and in 1971 (1 year after the operation). In 1971 and 1980, the castrated males were tested while under testosterone propionate treatment. The castrated and intact males did not differ in any measures of sexual behavior over the 10-year period, but both groups showed a decline in the percentage of tests with intromissions and ejaculations; a decline in the rates of contacting, mounting, and intromitting; and an increase in the latencies to contact, intromit, and ejaculate. In a second experiment, the sexual performances of old castrated and intact males were compared to those of young intact males (8 to 12 years). The intromission rate and the percentage of tests with intromissions were significantly greater in young males than in old intact males, but did not differ from values for old castrated males. The old castrated and old intact males did not differ from each other in these measures. Young males had a higher percentage of tests with ejaculation than either group of old males. We have concluded that old long-term-castrated rhesus males retain the potential to display sexual behavior at levels comparable to those observed in old intact males.

Age Factors↗
PubMed1975

In vitro pituitary responsiveness to gonadotropin-releasing hormone (LH-RH) in intact and castrated male and female rats.

The in vitro response of pituitaries isolated from both normal and 18-21 day post-castration male and female intact rats to incremental doses of synthetic gonadotropin-releasing hormone (LH-RH) has been investigated. Intact male pituitaries released luteinizing hormone (LH) maximally at the smallest dose of LH-RH (0.1 ng/ml) whereas intact female pituitaries released LH in a dose-response fashion. FSH release from intact male pituitaries was considerably greater than that from intact female pituitaries. As with LH, intact male pituitaries appeared maximally stimulated at 0.1 ng/ml of LH-RH. Intact female pituitaries did not release FSH until a 10 ng/ml dose of LH-RH was used. Male and female castrate pituitaries were more susceptible to LH-RH-induced LH and FSH release than were their intact counterparts, although this was more pronounced with regard to LH release. In addition castrate male pituitaries were more sensitive to lower doses of LH-RH than were castrate female pituitaries, this being most pronounced regarding LH release. Castrate female pituitaries released less FSH at the 100 ng/ml dose than at the 10 ng/ml dose, possibly indicating inhibition at these higher doses. In addition, pituitary extraction and serum from normal and castrate male and female rats were examined for LH and FSH content. LH content of castrated rat pituitaries of both sexes was considerably greater than that of their intact counterparts, as expected. However, castrate male pituitaries contained significantly less FSH than intact male pituitaries, whereas the opposite was true for the female groups. Serum LH and FSH levels were increased in the castrate groups with no difference between sexes. Serum from intact males contained considerably more FSH than did the serum from intact females.

Animals↗
PubMed1982

Ipsilateral hypothalamic deafferentation blocks the increase in serum FSH following hemi-castration.

In two experiments hypothalamic hemi-islands or sham surgeries were produced on the right side of prepubertal male rats with an extrudable Halàsz-type knife (1.5 mm radius). Animals were then sham castrated or else hemi-castrated on the contralateral or ipsilateral side with respect to brain surgery. Eight or 21 days later, hemi-castrated rats given sham knife cuts showed a significant increase in serum FSH, relative to sham animals with intact testes. Also, animals given hypothalamic hemi-islands and hemi-castrated on the contralateral side showed a significant increase in serum FSH comparable to that seen in hemi-castrated rats with sham brain surgeries. However, hypothalamic hemi-island rats which were hemi-castrated on the ipsilateral side failed to show an increase in serum FSH and were similar to sham operated controls with both gonads. Serum LH levels were comparable among all groups, verifying a clear dissociation between LH and FSH secretion associated with hemi-castration in prepubertal males. In addition, the differences between contralateral and ipsilateral hemi-castrated animals with identical unilateral brain surgeries strongly suggest that FSH release is, in part, under direct neural control. However, in a third experiment, differences in FSH release between ipsi- and contralateral hemi-castrated rats were not found in animals with hypothalamic hemi-islands on the left side of the brain. Thus the hypothalamus may be asymmetrically involved in various components of neuroendocrine control.

Afferent Pathways↗
PubMed2005

In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure: effects on the prostate and its response to castration in senescent C57BL/6J mice.

In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure inhibits ventral, dorsolateral, and anterior prostate development in C57BL/6 mice. To determine if prostatic abnormalities persist into senescence, mice born to dams given TCDD (5 mug/kg, po) or vehicle on gestation day 13 were examined at 100 and 510 days of age. Half the mice were castrated ten days prior to necropsy in order to assess androgen dependence, while the remaining mice were sham castrated. Effects of TCDD on the dorsolateral and anterior prostate of senescent sham-castrated mice were relatively subtle, whereas the ventral prostate was rudimentary or absent. Castration of vehicle-exposed mice caused far greater reductions in prostate lobe weights, epithelial cell height, and androgen-dependent gene expression (MP25 and probasin) in young mice than in senescent ones, while cell proliferation was decreased by castration in young mice and increased in senescence. Responses to castration were similar at 100 days of age in vehicle- and TCDD-exposed mice. At 510 days, however, TCDD-exposed mice were substantially more responsive to castration by most indices than vehicle-exposed mice. These results demonstrate that prostatic androgen dependence in mice declines substantially with age in several key ways, and that in utero and lactational TCDD exposure protects against this decline. Surprisingly, TCDD increased the incidence of cribriform structures in dorsolateral prostate ducts, from 2-3% in vehicle-exposed senescent mice to 16% in sham-castrated and to 7% in castrated senescent mice. Collectively, these results demonstrate that effects of in utero and lactational TCDD exposure on the prostate persist into senescence, and suggest that in utero and lactational TCDD exposure retards the aging process in the prostate. However, because cribriform structures are often considered to be associated with prostate carcinogenesis, these results also suggest that TCDD exposure early in development may increase susceptibility to prostate cancer.

Aging↗
PubMed1997

Anti-angiogenic treatment with linomide as adjuvant to surgical castration in experimental prostate cancer.

PURPOSE: Escape from "castration inhibition," be it surgical or chemically induced, is still the major problem in prostate cancer treatment. New agents that can be given as adjuvant therapy are needed. Linomide has demonstrated both anti-tumor and anti-angiogenic activity with little toxicity in the Dunning R-3327 rat prostate tumor system. Therefore it was deemed essential to study the efficacy of this drug in the adjuvant situation. MATERIALS AND METHODS: Linomide, roquinimex, was administered 3 times a week i.p. alone or in conjunction with castration to rats bearing the Dunning R-3327 PAP rat prostate tumor and its effect on tumor growth analyzed. Similar experiments, in which Linomide 25 mg./kg./day was given in the drinking water were carried out in rats with the Dunning R-3327 G tumor. The effect of treatment on blood vessel density and blood flow in the tumor was also assessed using an image analysis system. RESULTS: Linomide, 2.5 & 40 mg./kg., administered from the day after castration inhibited the regrowth of the Dunning R-3327 PAP tumors In addition, Linomide 40 mg./kg. administered after tumor regrowth occurred following castration(week 10) inhibited further tumor growth. Inhibition of tumor regrowth after castration was also found in the Dunning G tumor. When Linomide treatment was stopped regrowth of the tumors occurred, either in the same animal or on transplantation to new intact hosts, demonstrating that the tumor cells were still viable. Tumor blood vessel density was decreased both after castration and Linomide treatment alone, 40 and 32% respectively. On combination of castration and Linomide a 60% decrease in blood vessel density was found. This was significantly different from either of the two treatments given alone. The enhancement on combining castration and Linomide was confirmed by a further decrease in blood flow, from 19 and 22 to 12 ml. per minute/gm. tissue respectively. CONCLUSIONS: Linomide, an anti-angiogenic drug, inhibits escape from "castration inhibition".

Animals↗
PubMed1979

Testosterone-induced cell proliferation in the accessory sex glands of mice at various times after castration.

The proliferative response to testosterone in the accessory sex glands (seminal vesicle and coagulating gland) of castrated pale Balb/c mice has been examined by pulse and continuous thymidine-labelling experiments, and by the fraction of labelled mitoses technique. Progressive reductions in cellularity followed castration, and by varying the time elapsing between castration and the initiation of testosterone treatment, it was clear that the size of the response depended upon the number of cells in the tissue, relative to the normal complement. Interpretation of FLM data was difficult in periods where proliferative rates changed rapidly. We have attempted to explain the cell kinetic events by postulating a G0 compartment, form which cells are stimulated to enter the proliferative cycle before subsequently returning to an out of cycle state. It was thought unlikely that substantial changes in cell cycle time occurred. In both the accessory sex glands, the overall form of the continuous thymidine labelling curves showed that most proliferative cells entered DNA synthesis in a shorter time after stimulation at 14 days after castration than they did at 3 days after castration. The data were not consistent with cells moving deeper into G0 with time after castration. In the seminal vesicle almost all epithelial cells were potentially proliferative by 3 days after castration. In the coagulating gland only 30% were potentially proliferative at 3 days, increasing to 85% at 14 days after castration. However, such proportional increases represented much smaller changes in terms of absolute numbers of cells, because of a concomitant decline in cellularity from 3 to 14 days after castration.

Animals↗
PubMed1977

Myocardial lesions in rats fed rapeseed oil. II. Effects of castration.

The effects of castration on the incidence of myocardial lesions in rats were investigated in an experiment which included two factors: sex (entire males, castrated males, entire females and castrated (ovariohysterectomized) females) and diets (5% corn oil, 20% corn oil, and 20% Brassica napus var. Zephyr rapeseed oil). For 16 weeks, each of the 12 groups of 30 Sprague-Dawley rats, housed 2 per cage, were fed ad libitum the test oils incorporated in a semisynthetic diet. At each weighing, the mean body weights for each diet were highest in entire males followed by castrated males, castrated females, and entire females with all differences significant (P less than 0.05). The results indicated that castration did not influence cardiac fatty acid composition. The incidence of myocardial lesions in entire and castrated females and in castrated males was similar while significantly more entire males developed lesions (P less than 0.001). Rats fed a diet containing 20% Zephyr rapeseed oil showed a significantly (P less than 0.001) higher incidence of heart lesions than did rats fed diets containing 5% or 20% corn oil. Similarly, significantly (P less than 0.05) more rats fed the 20% corn oil diet had lesions than rats fed the 5% corn oil diet. The involvement of androgens in the formation of myocardial lesions is suggested, since castration significantly lowered the incidence in males but not in females.

Animals↗
PubMed1985

Castration of male rats reduces the capacity of granules isolated from the median eminence to secrete luteinizing hormone-releasing hormone in response to copper.

The effect of castration of male rats on the secretory function of median eminence area (MEA) granules containing luteinizing hormone-releasing hormone (LHRH) was examined, using copper as a test substance. LHRH granules, isolated from MEA of sham or castrated rats 1, 2, or 12 weeks postoperatively, were incubated with various concentrations of copper complexed to histidine (CuHis) and the kinetic constants of LHRH release estimated. CuHis-stimulated release of LHRH was found to be a saturable function of the concentration of CuHis. Castration did not alter the apparent Km for CuHis-stimulated release of LHRH; the Km being 3 and 16.9 microM copper for granules obtained from 1-2 weeks and 12 weeks sham-operated rats, respectively, and 3.7-5.6 and 10.2 microM copper for the granules of castrated rats, respectively. Moreover, castration did not alter the fractional amount of LHRH released in response to CuHis. In contrast, castration markedly reduced the actual amount of LHRH released in response to CuHis; the Vmax being 1,933 and 2,942 pg LHRH released/6 min/MEA for 1-2 weeks and 12 weeks sham-operated rats, respectively, and 782 and 757 pg for the castrated rats, respectively. Similarly, the LHRH content of the MEA of castrated rats was lower than that of the shams. These results are suggestive that castration reduces the capacity of the MEA granules to release LHRH in response to a secretion stimulus such as copper and that this is due not to alterations in the biochemical parameters underlying the release process itself but to a reduced level of MEA LHRH available for release.

Androgens↗
PubMed1982

Pituitary-testicular function in protein-deficient rats. Follicle-stimulating hormone hyperresponse to castration and supersensitivity of gonadotropin secretion to androgen negative feedback.

Previous studies have shown that weanling male rats fed a low protein diet ad libitum develop hypogonadotropic hypogonadism. Two unusual features of this state were 1) subnormal serum FSH in noncastrate rats but not in castrate rats, suggesting that FSH was being suppressed by a testicular factor, and 2) serum FSH increases after castration that were greater in protein-deficient rats than in controls. In the current study, protein-deficient rats showed FSH hyperresponse to castration, compared to either ad libitum or pair-fed controls, after periods of low protein feeding from 1-8 weeks and periods of castration from 1-8 weeks. FSH hyperresponse to castration was rapidly induced after the start of low protein feeding and was present whether castration was performed before or after low protein feeding was begun. In none of these circumstances did protein-deficient rats show LH hyperresponse to castration. Inhibin production of Sertoli cell cultures prepared from protein-deficient rats was less (P less than 0.02) than in ad libitum or pair-fed controls, suggesting that inhibin overproduction was not the cause of subnormal serum FSH in noncastrate protein-deficient rats. However, castrated rats fed a low protein diet were more sensitive to the negative feedback effects of testosterone on gonadotropin secretion than were ad libitum or pair-fed controls. We conclude that low serum gonadotropins in protein-deficient male rats may be related to hypersensitivity of these animals to the negative feedback effects of testosterone on gonadotropin secretion. In addition, FSH hyperresponse to castration, without corresponding LH hyperresponse, seems to be typical of protein deficiency, suggesting that protein deficiency may be a useful model for exploring the differential control of gonadotropin secretion.

Animals↗
PubMed2000

Prostatic luminal cell differentiation and prostatic steroid-binding protein (PBP) gene expression are differentially affected by neonatal castration.

BACKGROUND: Although normal prostatic development is androgen-dependent, the prostate continues to grow in the neonate despite castration. However, the manner in which neonatal growth of the prostate occurs, in the absence of the testis, remains largely unknown. The purpose of this study was to examine the differentiation of prostatic epithelial cells after neonatal castration. METHODS: Immunohistochemistry was utilized to detect the expression of differentiation products: basal-cell cytokeratin (CK 5), luminal-cell cytokeratin (CK 18), and prostatic steroid-binding protein (PBP), a ventral prostate-specific marker indicative of secretory function in luminal cells. The reverse transcription-polymerase chain reaction was used to detect transcription products of the three polypeptide subunits of PBP, designated C1, C2, and C3. Rats were castrated on day 5 after birth, and ventral prostates were collected on day 14. Dihydrotestosterone was injected (100 microg/animal every 2 days) in castrated animals to determine if PBP expression could be initiated by androgen. RESULTS: Although no major effects of castration were detected on the differentiation of stromal or basal cells (which differentiate prior to day 5), castration had a pronounced effect on luminal-cell differentiation. Castration inhibited PBP protein expression, but did not affect the expression of luminal-cell cytokeratin (CK 18) protein. Furthermore, castration reduced C1, C2, and C3 transcription. Androgen replacement to castrated animals allowed for the initiation of PBP expression, although its onset was delayed. CONCLUSIONS: These observations indicate that the testis is not necessary for prostatic luminal-cell differentiation, but is necessary for full expression of luminal-cell secretory phenotype. Furthermore, our study suggests that factors of testicular origin, in addition to androgen, are needed for proper timing of PBP expression. This investigation establishes that the cytological and the physiological differentiation of the rat prostate are differentially regulated.

Androgen-Binding Protein↗
PubMed2001

Castration in Gambel's and Scaled Quail: ornate plumage and dominance persist, but courtship and threat behaviors do not.

During the breeding season, testosterone in male birds is often linked to some secondary sexual ornaments, courtship behaviors, and intrasexual aggression. I examined the effect of castration on plumage expression in Gambel's Quail (Callipepla gambelii), a species in which males are highly ornate, and in Scaled Quail (C. squamata), an unornamented species. Using male pairs, each consisting of a castrate and a control, I also assessed whether castration affected (1) the behavior of males, (2) the mating decisions of females, or (3) the outcome of male-male competition. Castration did not alter the plumage of male Gambel's or Scaled Quail. In these species, and some other members of the avian order Galliformes, production of ornate plumage appears to be independent of testosterone. In contrast, castration reduced or eliminated courtship behaviors. Females almost never preferred castrated individuals. During male-male competition, castrates also exhibited lower rates of threat behaviors, which appear to be identical to those used during courtship. Castration did not, however, influence the outcome of male-male competition. Castrates of both species exhibited overt aggression (pecks, chases, displacement) and frequently won male contests. Such results suggest that certain types of aggressive behavior may be testosterone-independent. In both Gambel's and Scaled Quail, male body size correlated positively with dominant individuals.

Agonistic Behavior↗
PubMed1994

Expression of cytoplasmic and nuclear vasopressin RNA following castration and testosterone replacement: evidence for transcriptional regulation.

In order to determine the mechanism by which testosterone (T) regulates the expression of vasopressin (VP) in the bed nucleus of the stria terminalis (BNST) and medial amygdala (MA), in situ hybridization's were performed to measure the expression of cytoplasmic VP mRNA and nuclear VP RNA in Long-Evans rats that were castrated or T replaced for various lengths of time. One hour after castration, plasma T levels were significantly reduced and remained at this low level until the T was replaced in animals. Three hours after T replacement, plasma T levels were significantly elevated compared to those of control animals and returned to control levels within 9 h of replacement. Modulation of nuclear VP RNA expression by castration and T replacement was rapid. Six hours after castration, levels of nuclear VP RNA in the BNST and MA were reduced below limits of detection. Three hours after T replacement nuclear VP RNA expression was elevated in BNST and MA, achieving levels comparable to controls after 9 h of T replacement. In the BNST, the number of cells positively labeled by the nuclear VP RNA probe closely paralleled the changes observed in plasma T; in that 24 h after T replacement there was a significant increase in the number of cells positively labeled for nuclear VP RNA, with control levels returning 3 days later. Cytoplasmic VP mRNA expression in the BNST and MA, on the other hand, was slower to respond to both castration and T replacement than nuclear VP RNA. A significant change in the number of cells expressing cytoplasmic VP mRNA was observed approximately 3 days after castration in the BNST and 7 days after castration in the MA. The amount of labeling per cell of cytoplasmic VP mRNA responded more rapidly to the reduction of circulating T than the number of positively labeled cells. A significant decrease in grains/cell was observed 24 h after castration in the BNST and 3 days after castration in the MA. The number of cells expressing VP mRNA in both the BNST and MA required 3 days of T replacement to return to control levels; while the amount of labeling per cell required 7 days of replacement. Therefore, these data suggest that T's ability to regulate the expression of the VP mRNA occurs at least in part at the transcriptional level, since the expression of VP primary transcript was altered prior to changes in the hybridization signal for the cytoplasmic VP mRNA.

Amygdala↗