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PubMed1998

Castration differentially regulates nitric oxide synthase in the hypothalamus and pituitary.

Mammalian reproductive function is under control of the integrated hypothalamic-pituitary-gonadal (HPG) axis. Castration in male rats has been utilized as an effective tool to investigate hormonal interactions in the mammalian HPG axis. Recently, nitric oxide (NO) has been suggested to play a role in HPG hormonal regulation. In order to gain further insight into the function of the NO-NOS system in reproductive neuroendocrine control, particularly in the gonadal feedback regulation of the hypothalamic-pituitary unit, we examined steady state levels of nNOS mRNA, nNOS protein, and the important physiological index, NOS enzyme activity, of the intrinsic NOergic system in both hypothalamus and pituitary in castrated male rats and their sham-operated counterparts one week after surgery. In the pituitary, we found a significant four-fold increase in nNOS mRNA, p < 0.0003 compared to sham. Castration also resulted in a four-fold rise in pituitary nNOS protein, p < 0.02 compared to sham. Pituitary NOS enzyme activity was stimulated 2 fold, p < 0.003 after castration. In the hypothalamus, conversely, we observed no significant castration-modulated difference in either nNOS mRNA, nNOS protein or NOS enzyme activity. Thus, it appears that the hypothalamic NO-NOS system is either not required for hypothalamic adaptations to castration, although important in the release of LHRH under normal physiological conditions, or alternatively, the hypothalamus may become more sensitive to the effects of NO in the castrated state. In the pituitary, NO may attenuate the gonadotropin response to castration as a local balancing mediator.

Animals↗
PubMed1991

Septal arginine vasopressin (AVP) receptor regulation in rats depleted of septal AVP following long-term castration.

Arginine vasopressin (AVP) causes severe motor disturbances, including barrel rotations and myotonic/myoclonic convulsions, following repeated injections into either a lateral cerebral ventricle or the ventral septal area (VSA) of the rat brain. Because the AVP content of the rat septal area has been shown to be virtually eliminated following long-term castration, and because removal of a receptor ligand typically results in receptor upregulation and behavioral supersensitivity to the ligand, we tested the hypothesis that long-term castrated rats may be supersensitive to the motor actions caused by centrally injected AVP and may have upregulated septal AVP receptors. In these experiments, adult male Wistar rats were used 5 months after castration or, as controls, after sham castration. The effectiveness of long-term castration in eliminating AVP content of the VSA was indicated by the observation that a priming hypertonic saline stimulus (known to induce the central release of AVP and sensitize the rat brain) sensitized the brains of sham control rats but not of the castrated rats to the motor actions of a subsequent intracerbroventricular injection of AVP. The motor actions of centrally injected AVP, as well as septal AVP receptor characteristics (number and affinity), and AVP-stimulated phosphoinositide (PI) hydrolysis were then investigated in long-term castrated and sham control rats. Motor disturbances induced by either a first or a second injection of AVP were not greater in long-term castrated rats than in sham controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A transplantable rat Leydig cell tumour. 6. Effect of castration and hypophysectomy on tumour growth, morphology and plasma levels of pituitary hormones and testosterone.

Growth rate and morphology were studied in a transplantable rat Leydig cell tumour (H-540) grown in intact, castrated and hypophysectomized rats. The plasma levels of pituitary hormones and testosterone were measured in the same rats. The results can be summarized as follows: 1. The growth curves of tumours in intact and castrated rats were S-shaped and very similar during the observation period of three weeks. 2. In hypophysectomized rats, the onset and progression of tumour growth were delayed, compared with intact and castrated rats. 3. The thymidine labelling index as well as the size of the S and G2 phase compartments were decreased in tumours greater than 10 g compared with smaller tumours and tumours grown in hypophysectomized rats. 4. Testosterone concentrations in plasma correlate well with increasing tumour weight up to approximately 10-15 g in intact and castrated rats. 5. Plasma testosterone levels in tumour-bearing hypophysectomized rats were 7-fold higher than those of corresponding intact and castrated rats. 6. In castrated rats, suppression of LH production occurs by very small tumours (less than 2 g), whereas FSH levels show a gradual decrease with increasing tumour size. PRL production was independent of castration, tumour weight, and testosterone levels. 7. In spite of no major differences in cell morphology, the morphometric analysis revealed a reduction in tumour cell size and nuclear size in hypophysectomized rats compared with intact and castrated rats. It is concluded that pituitary hormones stimulate tumour growth, but surprisingly appear to reduce the secretion of testosterone from these tumours.

Animals↗
PubMed1975

Effect of castration on the smooth muscle cells of the internal sex organs of the rat: influence of the smooth muscle on the sympathetic neurons innervating the vas deferens, seminal vesicle and coagulating gland.

Wet weights of vas deferens, seminal vesicle and coagulating gland were reduced by almost 80 to 90% 10 weeks after castration. Endogenous norepinephrine content and dopamine-beta-hydroxylas activity of these tissues were also reduced to the same degree. One week after castration there was approximately a 50% loss in the weight of all three organs. However, this was accompanied by an equal reduction in norepinephrine content and dopamine-beta-hydroxylase activity only in the vas deferens. Two weeks later the degree of reductions in wet weight, norepinephrine content and dopamine-beta-hydroxylase activity was almost identical for all three organs. Treatment of 40-day castrate rats with testosterone (10 mg/kg s.c.) not only restored the wet weights of the internal sex organs to normal but their norepinephrine content and dopamine-beta-hydroxylase activity as well. Castration of immature rats (10-14 days old) resulted in retardation of growth of the vas deferens and seminal vesicle by 90-95%, and similar reductions in norepinephrin content and dopamine-beta-hydroxylase activity, when compared to the tissues of control littermates on the 90th postoperative day. Histological examination of normal and castrate rats indicated that, along with a reduction in epithelial cells, the smooth muscle cells of the vas deferens, seminal vesicle and coagulating gland was markedly reduce in size as well. Administration of testosterone completely reversed these changes. Furthermore, deoxyribonucleic acid content of the seminal vesicle and coagulating gland was reduced by 50% after castration and then restored to control level after testosterone treatment. Taken together, it seems that atrophy of the internal sex organs following castration is a combined effect of reduction in size and number of smooth muscle cells. Therefore, it is concluded that any alteration in the size of smooth muscle cells or loss of such cells of the internal sex organs indirectly influences their sympathetic nerves in such a manner that norepinephrine concentrations, and thereby the density of innervation, are maintained at normal levels.

Animals↗
PubMed1979

Fine structural studies of rat seminal vesicle in castrated and intact animals following estrogen treatment.

The effect of estradiol and/or testosterone upon secretion by seminal vesicle in castrated and intact rats was assessed in young adult Sprague-Dawley rats, using light microscopy (LM), transmission (TEM) and scanning (SEM)electron microscopy. Hormones were injected daily for ten days beginning ten days after castrations were performed. The normal rat seminal vesicle, as revealed by SEM, was characterized by a large saccular lumen with highly folded walls. Cell surfaces were covered with microvilli, or occasionally displayed a protruding, ruffled surface, sparsely covered with short microvilli. Cytology was normal in testosterone-treated animals. Estradiol treatment of castrated animals stimulated secretion by seminal vesicle epithelial cells as evidenced by the presence of normal secretory bodies, the presence of RER, and moderately hypertrophied Golgi complexes. These glands were not heavier than were glands from castrated, untreated animals, although the epithelial cells were significantly taller. Secretion was maintained in intact animals treated with estradiol, although glands were smaller and epithelial height was reduced. Estradiol and testosterone treatment in combination did not appear to have an additive effect on secretion, weight of the gland, or epithelial height. The following results support the hypothesis that estrogen-induced prolactin synthesis and release may be involved in the mechanism by which estradiol effected stimulation of seminal vesicle epithelium. Prolactin-treated, castrated animals exhibited focal areas of stimulated epithelium. In hypophysectomized animals (untreated controls), the seminal vesicle epithelium retained some secretory bodies and secretory fluid in the glandular lumen; epithelial height was taller than that in castrated controls. Estrogen treatment reduced the epithelial height to that of castrated controls; there was no evidence of secretion. This suggests that in the absence of anterior pituitary hormones, including prolactin, the stimulatory effect of estradiol on seminal vesicle epithelium was nullified. In adrenalectomized/castrated animals, estradiol treatment stimulated secretion in seminal vesicle epithelium just as in non-adrenalectomized/castrated animals. This indicates that the adrenal gland plays a non-essential role in the action of estrogen on seminal vesicle epithelium.

Adrenal Cortex Hormones↗
PubMed1975

The effects of castration and androgen replacement on song, courtship, and aggression in zebra finches (Poephila guttata).

Castration of adult male zebra finches (Poephila guttata, Estrildidae) reduces their singing rate and the tempo of song, but castrates continue to sing song identical in form to preoperative song. Injection or implantation of testosterone propionate (TP) but not of vehicle alone reverses the changes produced by castration. Castration or partial castration also reduces the frequency of courtship, copulation, and aggression. Androgen (TP) replacement reverses these changes, but control injections do not. The persistence of song after castration contrasts with the abolition of song by castration in other birds, and this may be related to the natural history of zebra finches.

Aggression↗
PubMed1980

Histochemical, autoradiographic and electron microscopic investigations of the renal proximal tubule of male and female rats after castration.

After castration of 90-day-old male and female rats, changes appear in the renal proximal tubule. A distinction can be made between early changes (up to 10th postoperative day) and later changes (20th-30th postoperative day). Between the 3rd and 5th day after castration the kidney of the females shows an increase in free estrogen receptors (biochemical studies) which are localized in the pars contorta of the proximal tubule (autoradiographic studies), while the male kidney shows a marked increase in urinary protein excretion up to the 10th day after castration. Proximal tubule changes detectable histochemically and electron microscopically do not appear until day 20 or 30 after castration. The results of castration are similar in segments S1 and S2. By days 20 and 30 after castration there is a decrease in the activity of lysosomal enzymes (acid phosphatase, acid beta-galactosidase). Electron microscopy shows a conspicuous decrease in the number of giant lysosomes (mainly in females) and apical vacuoles (mainly in males). A marked increase in the number of lysosomes is found in the S3 segment; females always have more lysosomes than males. The number of peroxisomes is also greatly increased; they appear circular in the females but can assume bizarre shapes in the males. Lipid droplets appear in the basal region of the tubule cell of segments S2 and S3 in the males. The sex differences are preserved in all segments even after castration and become even more pronounced in the S3 segment.

Animals↗
PubMed1977

Electrophysiological and contractile properties of the levator ani muscle after castration and testosterone administration.

Electrical and contractile properties of the levator ani muscle were studied in normal rats, in castrated rats and in castrated rats treated with testosterone. 2. No significant changes in the frequency of miniature end-plate potentials were found 6 months after castration. The frequency increased already 6 h after testosterone treatment; an increase of about 100% was observed after 7 days of testosterone treatment. 3. Castration led to a 2-fold increase of the input resistance of the muscle fibres. After 7 days of testosterone treatment the input resistance was only slightly higher than normal. 4. The weight of the muscle was decreased to 18% of the control value after 6 months castration. It increased to 46% after 7 days of testosterone treatment. 5. The muscles of castrated animals revealed a prolongation of contraction time and marked changes in maximal rate of tension development and half relaxation time. Partial recovery of these parameters was found after 7 days of testosterone treatment. 6. Long-term castration did not induce any denervation-like changes of action potential parameters, and no tetrodotoxin resistance was found in spite of marked muscle atrophy.

Anal Canal↗
PubMed1984

Isoprenaline-induced cell proliferation in mouse salivary glands: the effect of castration.

The proliferative response to isoprenaline in the submaxillary and parotid glands of the Balb/c mouse has been studied in the intact male and female, and also in the male castrated one month prior to stimulation. The hyperplastic response of the acinar cells has been monitored by serial measurements of the flash tritiated thymidine labelling index and the mitotic index. Castration caused the atrophy of the granular ducts in the submaxillary gland, and therefore an increased predominance of the acini. At one month after castration the acini occupied an area almost 1.5-fold greater than that of the granular ducts, but this was not as great as in the intact female gland where acini occupied twice the area of the granular ducts. Hyperplasia was induced by a single injection of isoprenaline (0.3 mM/kg body weight). The response of the submaxillary gland in the intact male and intact female was very similar, DNA synthesis commencing 21-24 h after stimulation and mitotic activity first noted after 33-36 h. On the other hand, in the submaxillary gland of the castrated male, DNA synthesis began after only 18-21 h and mitotic activity after only 27-30 h. A metaphase arrest experiment with vincristine confirmed the more prompt response in the castrated animals; between 33-36 h after isoprenaline injection, the rate of entry of cells into mitosis was 4 cells/100 cells/h in the castrated group but only 0.4 cells/100 cells/h in the intact males. Thus castration appears to bestow a unique state of responsiveness upon the submaxillary gland to isoprenaline stimulation. The mechanisms underlying this change are not yet understood, for it is paradoxical that atrophy of a structural component rich in specific protein growth factors can alter the format of isoprenaline-induced hyperplasia in acinar cells that produce secretory glycoproteins.

Animals↗
PubMed1984

Rate-determining factors for ethanol metabolism in fasted and castrated male rats.

The effects of castration and fasting upon the alcohol elimination rate, liver alcohol dehydrogenase (LADH) maximum activity (Vmax), and hepatic concentrations of ethanol, acetaldehyde, and free NADH during ethanol oxidation were examined in male Wistar rats. Castration increased the Vmax of LADH and, to a lesser extent, the alcohol elimination rate in vivo. On the other hand, fasting reduced the Vmax of LADH and the alcohol elimination rate in sham-operated and castrated rats but it did not nullify the effect of castration. Castration produced small but significant changes in the hepatic concentrations of ethanol, acetaldehyde and free NADH in fed rats during ethanol oxidation. Fasting also caused significant increases in the concentration of free NADH during alcohol oxidation in both the sham-operated and castrated groups. The ratio of the steady-state velocities of LADH in situ to the maximum velocities of LADH (v/Vmax) under the different experimental conditions was calculated by using the steady-state rate equation for the enzyme mechanism of rat LADH and its kinetic constants. The calculated v/Vmax ratios were 50-62%, indicating that LADH activity was limited to about the same extent by its substrates and products under these conditions and that the changes in alcohol elimination rates produced by fasting and castration mainly reflected changes in the Vmax of LADH. The calculated steady-state velocities in situ (v) were 14-28% lower than the measured rates of alcohol elimination in vivo. The extent of agreement is probably acceptable in view of the assumptions needed to determine the free NADH concentration in liver and the existence of non-LADH-related processes for alcohol elimination in vivo.

Alcohol Dehydrogenase↗
PubMed1993

Effect of castration on hyperlipidemic, insulin resistant JCR:LA-corpulent rats.

The JCR:LA-cp rat exhibits an obese, insulin resistant, hyperlipidemic syndrome. Obese male rats, only, develop atherosclerosis and ischemic myocardial lesions. The obese males have a greater hyperinsulinemia, but the obese females have a much greater hypertriglyceridemia due to hypersecretion of very low density lipoprotein (VLDL). Obese rats of both sexes were surgically castrated at 6 weeks of age to study the influence of testosterone and estrogen secretion on the sexual dimorphism of metabolism and disease in this strain. Castration had no effect on body weight or food consumption up to 16 weeks of age. Castrated male rats had significantly improved glucose tolerance, but a doubled serum triglyceride concentration. Castrated female rats showed approximately halved triglyceride levels. The distribution of the triglyceride molecular species was altered in the castrated male rats to resemble that of the females in which there was no change with castration. The effects suggest that testosterone may inhibit hepatic triglyceride secretion and promotes insulin insensitivity. Estrogen appears to exacerbate hepatic hypersecretion of VLDL. Castration had no effect on myocardial lesion frequency in 9-month-old rats of either sex. This implies that estrogen does not exert a direct protective effect against cardiovascular disease in this animal model.

Animals↗
PubMed1983

Effects of delta 9-THC and castration on behavior and plasma hormone levels in male mice.

Gonadectomy resulted in a rapid increase in plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, but had no consistent effects on plasma prolactin (PRL) and growth hormone (GH) levels. In castrated males, oral administration of THC (50 mg/kg) significantly increased plasma LH levels within hours following surgery and again from 3 to several weeks post-castration, while THC treatment decreased LH levels between 1 day and 2 weeks postcastration. Administration of THC to 12-hour sham castrates significantly increased plasma LH levels. Plasma FSH, PRL and GH levels were either reduced or unchanged by THC. Administration of THC significantly reduced levels of gonadotropins, PRL and GH in intact males. In additional studies, we examined the influence of THC on the negative feedback response of the anterior pituitary to gonadal steroids. In testosterone propionate (TP)-treated castrated males, concomitant administration of THC increased plasma testosterone (T) and LH at 20 min, while plasma FSH levels were elevated after 60 min. In contrast, in intact TP-treated mice, concomitant THC exposure reduced plasma T levels except at 60 min, when plasma LH levels were significantly increased. Testosterone replacement failed to restore copulatory behavior in castrated mice given a single dose (50 mg/kg) of THC. In fact, acute THC administration to these TP-treated castrates resulted in marked sedation, which was not observed in intact mice given the same dose of THC in an earlier study. The present findings indicate that the effects of acute THC treatment on pituitary gonadotropin release is dependent upon the time after castration. Furthermore, THC administration can suppress copulatory behavior even in animals whose peripheral T levels have been maintained. Effects of THC on plasma androgen levels in animals injected with TP suggest that THC can alter the metabolism or target tissue response to gonadal steroids.

Animals↗
PubMed1988

The response of autonomic receptors to castration and testosterone in the urinary bladder of the rabbit.

The effects of castration and testosterone on the autonomic receptor density and contractility in the urinary bladder smooth muscle of male rabbits were compared to untreated animals. Four groups of rabbits were studied over a similar time span with Group 1 animals serving as the untreated controls. Two groups (Groups 2 and 3) were castrated 28 days prior to sacrifice, Group 2 animals received corn oil for 14 days, and Group 3 animals received testosterone, 10 mg./day, for 14 days. The Group 4 animals were non-operated and received testosterone 10 mg./day for 14 days. Ligand saturation binding studies for alpha adrenoceptors in the bladder base and proximal urethra were performed with [3H]dihydroergocryptine ([3H]DHE). Muscarinic cholinergic receptors (MChR) were assayed with [3H]quinuclidinyl benzilate ([3H]QNB) and beta adrenoceptors with [125I]iodocyanopindolol ([125I]CYP) on the detrusor smooth muscle. Castrated Group 2 animals showed no significant change in receptor density with either [3H]QNB or [125I]CYP in detrusor muscle, but did exhibit a significant reduction (59%) of alpha adrenoceptors in the bladder base-urethra. The testosterone treated castrate and testosterone treated non-operated animals had significant increases in the MChR density, but no change in the alpha adrenergic, or beta adrenergic receptor density as compared to untreated controls. Cumulative dose response contractile studies were performed with carbachol on detrusor muscle strips and with phenylephrine on bladder base strips in isolated organ baths. The contractile studies on muscles from Groups 1, 2 and 3 showed no change in the ED50 or maximal contractile strength between control, castration or testosterone treated castrated animals. The ratio of wet bladder weight as compared to total body weight between each of the treatment groups showed a slight increase in both of the testosterone treatment groups. It was concluded that castration down regulates the alpha adrenergic receptors of the bladder base, while testosterone treatment increases the density of MChRs, and increases the ratio of the bladder to total body weight. Although no contractile changes were observed in the bladder base tissue it is conceivable that longer chronic testosterone deficits might ultimately affect the bladder outlet resistance in the male because of the reduced alpha adrenergic receptor density.

Animals↗
PubMed1985

Down regulation of the muscarinic cholinergic receptor of the rat prostate following castration.

Prostatic secretion is dependent upon the integrity of the endocrine and autonomic nervous systems and is dramatically influenced by muscarinic cholinergic analogs. In this study, we have used radioligand receptor binding methods on whole tissue homogenates and slide mounted tissue sections of rat prostate to determine whether androgens regulate the density of muscarinic cholinergic receptors in the prostate. The muscarinic cholinergic receptor binding affinities (Kd) of [3H] N-methylscopolamine in prostatic homogenates obtained from intact, castrate, and castrate rats receiving testosterone replacement (castrate + T) were similar (0.07 to 0.10 nM). The muscarinic cholinergic receptor binding capacity decreased 73 per cent following castration. Testosterone administration restored the density of muscarinic cholinergic receptors in castrate rats to intact levels. In order to ensure that the loss of receptor density was not due to a decrease in the epithelial: stromal cell ratio, the number of muscarinic cholinergic receptors per unit area of epithelium was determined in the 3 treatment groups using autoradiography on slide mounted tissue sections. The density of muscarinic cholinergic receptors in a unit area of epithelium was decreased 91 per cent following castration. Testosterone administration restored the density of muscarinic cholinergic receptors in the castrate rats to intact levels. The modulation of neurotransmitter receptors by steroid hormones may be a mechanism by which sex steroids regulate biological responsiveness of target tissues.

Androgens↗
PubMed1970

The influence of thyroactive substances on the induction of cervico-vaginal tumours in intact and castrate rats.

The effect of the administration of L-thyroxine and of methylthiouracil alone, together, in combination with stilboestrol or in the perinatal period on the induction of cervico-vaginal tumours by weekly local applications of DMBA was investigated in intact and castrate rats and compared with carcinogenesis in animals not additionally treated.In intact rats the rate of sarcoma induction is accelerated by methylthiouracil, delayed and reduced by methylthiouracil plus L-thyroxine and delayed by perinatal injection of either L-thyroxine or methylthiouracil. In castrates sarcoma induction is accelerated and increased by L-thyroxine, methylthiouracil and by combination of either substance with stilboestrol; it is accelerated but not significantly increased by combined treatment with the thyroactive compounds.The incidence of epithelial neoplasms is accelerated and increased in intacts and in castrates by methylthiouracil. This effect is slightly reduced in intacts but potentiated in castrates by additional stilboestrol treatment as well as by administration of L-thyroxine plus methylthiouracil.The incidence of sarcomas is significantly greater in intact than in spayed rats not additionally treated, greater in castrates than in intacts given L-thyroxine ± stilboestrol and not significantly different in intacts and castrates with any of the other additional medications. For epithelial tumours the incidence is low and similar in both groups without additional treatment, greater in spayed than intact animals given methylthiouracil plus stilboestrol or plus L-thyroxine.The influence of the thyroactive compounds on the induction of epithelial and sarcomatous tumours is not correlated with their effect on gain in body weight nor on growth of the stroma and of the epithelium of the vagina, cervix and uterus. Changes induced in the thyroid gland and the hypophysis are not correlated with those on carcinogenesis.Central and local factors may account for the differential response in carcinogenesis of intacts and castrates as well as of the epithelial and connective tissue of the cervico-vaginal tract to medication with thyroactive compounds.

Animals↗
PubMed1989

Treatment of problem behaviour in dogs and cats by castration and progestagen administration: a review.

Treatment of problem behaviour in companion animals by castration and progestagen administration is reviewed. In male dogs castration is effective in eliminating roaming and, to a lesser extent, mounting, urine marking and intermale aggression. Spraying, roaming and fighting behaviour in cats disappear almost completely after castration. In the latter species prepubertal castration does not seem to be more effective in preventing this problem behaviour than postpubertal castration is in eliminating it. In dogs, intermale aggression, urine marking, mounting and roaming have been treated successfully with progestagens; in cats the same treatment has been successful in decreasing fighting and roaming. There are no reports on the ethical aspects or on adverse side effects of castration. For progestagens a wide range of undesirable side effects have been described. The results of both castration and progestagen therapy differ in the various studies. The underlying mechanism(s) of progestagen influence on behaviour are not understood. Therefore, future research on this topic is necessary.

Animals↗
PubMed1984

Neonatal castration of male and female rats affects luteinizing hormone responses to estrogen during adulthood.

We examined the positive and negative feedback effects of estradiol (E2) on luteinizing hormone (LH) and prolactin (Prl) secretion in adult male and female rats which were gonadectomized within 24 h after birth (long-term castrates) and compared these responses to those elicited by E2 in short-term castrated (7 days) adult males and females. The high serum E2 did not reduce the elevated serum LH concentrations in long-term castrates until 4 days of treatment. Also, only after negative feedback was established were the positive feedback actions of E2 observed. In contrast, Prl surges were observed after 2 days of E2, and baseline Prl serum levels were elevated by Day 3 of E2 in long-term castrated male and female rats. Some long-term castrates lacked both LH and Prl surges, and E2 was ineffective in altering basal gonadotropin secretion in these animals. Short-term castrated males had elevated serum Prl levels but no Prl surges. Seemingly, when the hypothalamus is deprived of estrogen or androgen from birth to adulthood, an equal percentage of males and females become refractory to the positive feedback effects of estrogen during adulthood. Thus, it is difficult to separate castration effects from those which may be produced by the endogenous androgen secreted during the first 26 h of life.

Aging↗
PubMed2004

Hormone treatment facilitates penile erection in castrated rats after sleep deprivation and cocaine.

Sleep deprivation is associated with cocaine-enhanced genital reflexes in male rats, and castration of the male rat causes a decline in sexual behaviour, which can be reversed by hormone administration. We conducted two experiments to determine whether sleep deprivation and cocaine administration could also induce spontaneous penile erection in castrated rats after hormonal treatment (testosterone, progesterone and oestradiol). Different doses of hormones or vehicle were administered to rats during the 4-day period of sleep deprivation, and in home-cage control rats. Testosterone did not restore penile erection in castrated sleep-deprived rats. Progesterone triggered penile erection, and 100 mg/day of progesterone induced the highest proportion of rats displaying penile erection, and restored the frequency of penile erection observed in noncastrated sleep deprived rats. Penile erection was absent in vehicle as well as oestradiol-treated sleep-deprived castrated rats. Whereas sleep deprivation increased progesterone concentrations in noncastrated rats, sleep deprivation decreased progesterone concentrations in castrated rats. Corticosterone concentrations were lower in the castrated sleep-deprived rats than in respective control group. These data show that progesterone treatment facilitates penile erection in sleep deprived-cocaine castrated rats.

Animals↗