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PubMed2006

Bone marrow failure in male rats following trauma/hemorrhagic shock (T/HS) is mediated by mesenteric lymph and modulated by castration.

Bone marrow (BM) suppression occurs following trauma/hemorrhagic shock (T/HS) in experimental animals as well as following severe injury in humans. Although the pathophysiology of BM suppression remains poorly understood, mesenteric lymph is thought to play an important role in T/HS-induced BM suppression; however, the direct effect of mesenteric lymph on BM in vitro has never been studied. In addition, recent studies in rats have also shown that female and castrated male rats are protected against T/HS-induced BM failure. We therefore hypothesized that mesenteric lymph is a source of factor(s) causing direct BM suppression and that the effects of mesenteric lymph are gender dependent. To test this hypothesis, we subjected noncastrated (NC) and castrated (C) male and proestrus female rats to T/HS or trauma sham shock (T/SS). Mesenteric lymph collected 3 h postshock was plated (4% v/v) with BM cells collected from unmanipulated male or female rats for granulocyte-macrophage colony-forming units (CFU-GM) and erythroid burst-forming units (BFU-E) colony growth. The T/HS lymph collected from NC-male rats but not from female rats caused a 50% inhibition of CFU-GM and BFU-E colony growth compared with cells cultured without lymph (P < 0.05 versus all other groups (ANOVA + Tukey). T/HS lymph collected from C-male rats also caused no significant inhibition of CFU-GM and BFU-E colony growth compared with cells cultured without lymph. Female and male BM progenitor cells had a similar response to mesenteric lymph from all groups tested. These results show that mesenteric lymph from NC-male rats suppresses CFU-GM and BFU-E progenitor growth in vitro, whereas the lymph from C-male and female rats did not. The effects of mesenteric lymph were the same regardless of whether the target BM was from male or female rats. The results therefore indicate that BM failure in male rats is directly mediated by factors present within the mesenteric lymph that appear to be modulated by castration, and protection against BM failure in female rats occurs at a systemic rather than a local level. Further studies are needed to elucidate potential therapeutic effects of lymph manipulation in hematopoiesis after injury.

Animals↗
PubMed1988

Effects of androgens, prolactin and bromocriptine on seminal vesicular enzymes of the pyruvate malate cycle involved in lipogenesis in castrated mature monkeys, Macaca radiata.

The interaction of androgens and prolactin, the major factors regulating the male accessory sex organs, on the specific activity of seminal vesicular enzymes of the pyruvate/malate cycle were studied in castrated mature monkeys. Castration decreased the activity of these enzymes, including NADP+ isocitrate dehydrogenase, ATP citrate lyase, malate dehydrogenase, malic enzyme and fatty acid synthase. Testosterone propionate (TP)/dihydrotestosterone given as replacement to castrates increased the activity of all these enzymes, except for malate dehydrogenase. Prolactin restored normal activity of ATP citrate lyase, malic enzyme and fatty acid synthase but not of isocitrate dehydrogenase and malate dehydrogenase (MDH). Prolactin had a specific control over MDH. Moreover, when prolactin was combined with androgens a further stimulatory influence was observed on fatty acid synthase activity. In order to prove the direct influence of prolactin on enzymes of the pyruvate/malate cycle, bromocriptine was administered and this inhibited all of the enzymes. Thus prolactin was found to have a direct, as well as a synergistic, action with androgens on enzymes of the pyruvate/malate cycle in the seminal vesicles of monkeys.

ATP Citrate (pro-S)-Lyase↗
PubMed1991

Effects of castration, Depo-testosterone and cyproterone acetate on lymphocyte T subsets in mouse thymus and spleen.

The effects of testosterone on the relative proportion of Thy 1.2, CD4 (L3T4) and CD8 (Lyt-2) cells in thymus and spleen were studied after castration and administration of Depo-testosterone (DT) separately or together with cyproterone acetate (CA) (an antiandrogen) in BDF1 mice. Injection of 0.5 mg/100 g body weight of DT during 2 weeks decreased significantly the number and proportion of double positive (DP) (CD4+ CD8+) and increased the percentage of single positive (SP) CD4+ (CD4+ CD8-), whereas there was a slight decrease in the Thy 1.2+ cells in the thymus. In parallel, we observed an increase in CD8+ (CD4- CD8+) cells in the spleen. The androgen deprivation after 3 weeks of castration induced a decrease in the percentage of CD4+ cells in thymus and both CD4+ and CD8+ cells in spleen. Injection of CA (0.5 mg/100 g body weight) had the same qualitative effects as DT on the proportion of lymphocyte T subsets in castrated mice. However, the combined activities of DT and CA were greater than either alone. These data indicate the main role of testosterone in the distribution of CD4+ and CD8+ cells in male mice. The similar effects of CA and DT in the lymphoid organs may suggest a difference between androgen receptors of sexual and lymphoid organs.

Androgen Antagonists↗
PubMed1993

Regional variation in gamma-aminobutyric acid turnover: effect of castration on gamma-aminobutyric acid turnover in microdissected brain regions of the male rat.

This study compared the turnover of GABA neurons in different brain areas of the male rat and examined the effect of castration on GABA turnover in regions of the brain associated with the control of gonadotropin secretion. To estimate GABA turnover, GABA was quantified by HPLC in microdissected brain regions 0, 30, 60, 90, and 120 min after inhibition of GABA degradation by aminooxyacetic acid (100 mg/kg, i.p.). GABA accumulation was linear in all areas for 90 min (p < 0.01), and GABA turnover was estimated as the slope of the line formed by increased GABA concentration versus time, determined by linear regression. There was considerable regional variation both in the initial steady-state concentrations of GABA and in the rates of GABA turnover. Of 10 discrete brain structures, GABA turnover was highest in the medial preoptic nucleus and lowest in the caudate nucleus. Turnover times in the terminal fields of known GABAergic projection neurons ranged sevenfold, from 2.6 h in the substantia nigra to 0.4 h in the lateral vestibular nucleus. The effect of castration on GABA turnover in 13 microdissected brain regions was investigated by measuring regional GABA concentrations before and 30 min after injection of aminooxyacetic acid in intact rats or 2 or 6 days postcastration. Following castration, steady-state GABA concentrations were increased, and GABA turnover decreased in the diagonal band of Broca, the medial preoptic area, and the median eminence. GABA turnover increased in the medial septal nucleus and was unaffected in the cortex, striatum, and hindbrain. These results are consistent with the hypothesis that testosterone negative-feedback control of luteinizing hormone-releasing hormone involves steroid-sensitive GABAergic neurons in the rostral and medial basal hypothalamus.

Aminooxyacetic Acid↗
PubMed1994

Acute ethanol exposure suppresses the repair of O6-methylguanine DNA lesions in castrated adult male rats.

Alcohol has clearly been associated with an increase of cancers in numerous tissue, including the respiratory tract, colon, rectum, liver, but especially the esophagus, larynx, pharynx, and mouth. Alcohol alone has not been shown to be a mutagen until it is converted to acetaldehyde and, therefore, alcohol presumably acts as a cocarcinogen. Previous data has shown that alcohol concentrations of 2% or greater inhibits DNA repair, and in light of the widespread consumption of alcoholic beverages with alcohol contents ranging from 4 to 5% (beer and wine coolers) to 50% (whiskey), interest in determining the mechanism(s) responsible for alcohol-induced carcinogenesis has heightened. Although previous studies, in intact rats, have investigated the effects of chronic alcohol exposure on some aspects of DNA repair, we have begun to address the effects of acute or "binge" alcohol exposure on mammalian DNA repair. Toward this end, we report the inhibition of O6-methylguanine-DNA methyltransferase (MGMT) by a single intraperitoneal injection of 30% ethanol in adult male castrated rats. This inhibition lasted for at least 24 hr. We also observed a dose-response effect of ethanol on MGMT activity, again only in the castrated rats. The finding of ethanol's effect on MGMT activity in castrated and not intact rats implies a hormonal component of MGMT DNA repair response, which has only been alluded to in past research.

Animals↗
PubMedDate not supplied

Laparoscopic cryptorchid castration in standing horses.

OBJECTIVE: This article describes a new technique for laparoscopic cryptorchid castration in standing horses. STUDY DESIGN: Prospective study. ANIMALS OR SAMPLE POPULATION: Eight horses aged 11 months to 3 years and weighing between 300 and 643 kg. METHODS: Food was withheld for 24 to 36 hours, and then horses were sedated with detomidine HCl (0.02 to 0.03 mg/kg) and butorphanol tartrate (0.02 mg/kg). The paralumbar fossa region was desensitized with 2% mepivacaine in an inverted "L" pattern and caudal epidural anesthesia was administered with either xylazine (0.18 mg/kg diluted to 10 to 15 mL with 0.9% sodium chloride) or a combination of 2% mepivacaine and xylazine (0.18 mg/kg). Initial laparoscopic exploration was performed from the left flank; in three horses, right flank laparoscopy was needed to complete the procedure. The spermatic cord was ligated within the abdomen with one or two sutures of 0 polydioxanone suture, and the testis or testes removed through a flank incision. RESULTS: In five horses with no palpably descended testes, standing laparoscopy was the only procedure performed, whereas in two horses, the abdominal testis was removed laparoscopically, and the descended testis was removed under short acting anesthesia. In one horse, with nonpalpable testes, it was determined by laparoscopic observation that the testes were in the inguinal canal, and castration was performed under general anesthesia. No surgical or postoperative complications were noted. The right side of the abdomen, and especially the right vaginal ring, could be easily observed from the left side by passing the laparoscope through a small perforation in the mesocolon of the descending colon or by elevating the descending colon with an instrument or by use of an arm in the rectum. CONCLUSIONS: The standing laparoscopic approach combined with or without short-acting anesthesia to remove the descended testis is easily performed. CLINICAL RELEVANCE: This approach will provide surgeons with another option to castrate cryptorchid stallions.

Anesthesia, General↗
PubMed2005

Effects of icariin on erectile function and expression of nitric oxide synthase isoforms in castrated rats.

AIM: To investigate the effect of icariin on erectile function and the expression of nitric oxide synthase (NOS) isoforms in castrated rats. METHODS: Thirty-two adult male Wistar rats were randomly divided into one sham-operated group (A) and three castrated groups (B, C and D). One week after surgery, rats were treated with normal saline (groups A and B) or oral icariin (1 mg/[kg.day] for group C and 5 mg/[kg.day] for group D) for 4 weeks. One week after treatment, the erectile function of the rats was assessed by measuring intracavernosal pressure (ICP) during electrostimulation of the cavernosal nerve. The serum testosterone (ST) levels, the percent of smooth muscle (PSM) in trabecular tissue, and the expression of mRNA and proteins of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS) and phosphodiesterase V (PDE5) in corpus cavernosum (CC) were also evaluated. RESULTS: ICP, PSM, ST and the expression of nNOS, iNOS, eNOS and PDE5 were significantly decreased in group B compared with those in group A (P 0.01). However, ICP, PSM and the expression of nNOS and iNOS were increased in groups C and D compared with those in group B (P 0.05). Changes in ST and the expression of eNOS and PDE5 were not significant (P 0.05) in groups C and D compared with those in group B. CONCLUSION: Oral treatment with icariin ( 98.6 % purity) for 4 weeks potentially improves erectile function. This effect is correlated with an increase in PSM and the expression of certain NOS in the CC of castrated rats. These results suggest that icariin may have a therapeutic effect on erectile dysfunction.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1988

Stress responses in lambs docked and castrated surgically or by the application of rubber rings.

A comparative study has been made in lambs 3 to 6 weeks of age of the behavioural responses and changes in plasma immunoreactive beta-endorphin (ir beta-endorphin) and cortisol after docking or docking plus castration by the application of rubber rings or by surgery. The use of rubber rings on lambs at this age was characterised by very agitated behaviour indicative of considerable distress for a period of up to 1 h. In contrast, surgery was accompanied by some post-operative shock exhibited by reduced exploratory and social behaviour, at least in the lambs exposed to docking plus castration. In the latter group there were highly significant increases in both plasma ir beta-endorphin and cortisol concentrations that may be consistent with the induction of stress-induced analgesia. We conclude that surgery caused less distress than the rubber rings, and is therefore preferable for docking and castration of lambs 3 to 6 weeks of age.

Animals↗
PubMedDate not supplied

Effects of castration on peritoneal fluid in the horse.

Twenty-four clinically normal horses were castrated by routine methods. Peritoneal fluid was collected prior to castration and at 1, 3, 5, and 7 days postcastration. Peritoneal fluid was collected on days 9 and 11 if nucleated cell (NC) counts were still markedly elevated on day 7. Peritonitis, defined as NC counts greater than 10,000/microliters, was evident in 15 horses following castration. Mean NC counts peaked on day 5 but were less than 10,000/microliters for 74% of the horses by day 7, and 90% of the horses by day 9. One horse had a NC count greater than 60,000/microliters on day 11 when sampling ended. Postcastration peritoneal fluid was obviously blood-tinged in 21 horses. Peak RBC counts occurred on day 3 but markedly decreased by day 5. Elevated peritoneal RBC counts correlated well with elevated NC counts (P less than 0.001). Horses with peritonitis tended to have fever (P less than 0.05). Other clinical signs of peritonitis were not apparent.

Animals↗
PubMed1990

Visceral prolapse after castration in the horse: a review of 18 cases.

During a 10 year period, 18 horses were treated surgically because of visceral prolapse after castration. Surgery was successful in six cases of omental prolapse and in eight out of 12 cases of intestinal prolapse. To minimise the risk of visceral prolapse, the authors prefer half-closed castration, with proper ligation of the parietal vaginal tunic, to open castration. If adequate treatment is started promptly, prognosis in cases of visceral prolapse is favourable.

Animals↗
PubMed1987

Luteinizing hormone release in intact and castrate rams is altered with immunoneutralization of endogenous estradiol.

Changes in the dynamics of luteinizing hormone (LH) release in the adult ram following immunoneutralization of endogenous estradiol were investigated. Castrate rams were actively immunized against estradiol-6-bovine serum albumin for 7 months and then their patterns of episodic LH release and LH response to multiple injections of gonadotropin-releasing hormone (GnRH, two 5-micrograms doses given iv 2 h apart) were assessed (April). In comparison with control rams immunized against rabbit gamma globulin, estradiol-immunized rams (antibody titre approximately 1:5000) exhibited more frequent LH releases (11.7 +/- 0.3 vs. 9.3 +/- 0.8 pulses/8 h, P less than 0.05) and a greater LH response to the first GnRH injection (peak delta value 190 +/- 8 vs. 130 +/- 25 ng/mL, P less than 0.01). Estradiol antiserum collected from the castrate rams was used in the passive immunization of intact rams (antibody titre approximately 1:200) for 1 month (beginning mid-July). Although episodic LH release was always similar for control and immunized rams, testosterone levels in the latter group increased approximately 150%. In contrast with the castrate ram response, GnRH treatment (two 5-micrograms doses given iv 80 min apart) produced a "self-priming" effect on LH release in the intact rams, an effect that was dampened with estradiol immunoneutralization. Consequently, peak 2:peak 1 ratios for delta value and 80-min mean incremental increase were much smaller (P less than 0.01) for the immunized rams (approximately 2:1 vs. 4:1 for the control rams).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Effect of medical castration on CD4+ CD25+ T cells, CD8+ T cell IFN-gamma expression, and NK cells: a physiological role for testosterone and/or its metabolites.

The higher prevalence of autoimmune disease among women compared with men suggests that steroids impact immune regulation. To investigate how sex steroids modulate cellular immune function, we conducted a randomized trial in 12 healthy men aged 35-55 yr treated for 28 days with placebo, a GnRH antagonist, acyline to induce medical castration, or acyline plus daily testosterone (T) gel to replace serum T, followed by a 28-day recovery period. Serum hormones were measured weekly and peripheral blood lymphocytes (PBLs) were collected biweekly for analyses of thymus-derived lymphocyte (T cell) subtypes and natural killer (NK) cells. Compared with the other groups and to baseline throughout the drug exposure period, men receiving acyline alone had significant reductions in serum T (near or below castrate levels), dihydrotestosterone, and estradiol (P < 0.05). Medical castration significantly reduced the percentage of CD4+ CD25+ T cells (P < 0.05), decreased mitogen-induced CD8+ T cell IFN-gamma expression, and increased the percentage of NK cells without affecting the ratio of CD4+ to CD8+ T cells and the expression of NK cell-activating receptor NKG2D or homing receptor CXCR1. No changes in immune composition were observed in subjects receiving placebo or acyline with replacement T. These data suggest that T and/or its metabolites may help maintain the physiological balance of autoimmunity and protective immunity by preserving the number of regulatory T cells and the activation of CD8+ T cells. In addition, sex steroids suppress NK cell proliferation. This study supports a complex physiological role for T and/or its metabolites in immune regulation.

Adult↗
PubMed2006

Mathematical model for the androgenic regulation of the prostate in intact and castrated adult male rats.

The testicular-hypothalamic-pituitary axis regulates male reproductive system functions. Understanding these regulatory mechanisms is important for assessing the reproductive effects of environmental and pharmaceutical androgenic and antiandrogenic compounds. A mathematical model for the dynamics of androgenic synthesis, transport, metabolism, and regulation of the adult rodent ventral prostate was developed on the basis of a model by Barton and Anderson (1997). The model describes the systemic and local kinetics of testosterone (T), 5alpha-dihydrotestosterone (DHT), and luteinizing hormone (LH), with metabolism of T to DHT by 5alpha-reductase in liver and prostate. Also included are feedback loops for the positive regulation of T synthesis by LH and negative regulation of LH by T and DHT. The model simulates maintenance of the prostate as a function of hormone concentrations and androgen receptor (AR)-mediated signal transduction. The regulatory processes involved in prostate size and function include cell proliferation, apoptosis, fluid production, and 5alpha-reductase activity. Each process is controlled through the occupancy of a representative gene by androgen-AR dimers. The model simulates prostate dynamics for intact, castrated, and intravenous T-injected rats. After calibration, the model accurately captures the castration-induced regression of the prostate compared with experimental data that show that the prostate regresses to approximately 17 and 5% of its intact weight at 14 and 30 days postcastration, respectively. The model also accurately predicts serum T and AR levels following castration compared with data. This model provides a framework for quantifying the kinetics and effects of environmental and pharmaceutical endocrine active compounds on the prostate.

Androgens↗
PubMed2004

NE-10 neuroendocrine cancer promotes the LNCaP xenograft growth in castrated mice.

Increases in neuroendocrine (NE) cells and their secretory products are closely correlated with tumor progression and androgen-independent prostate cancer. However, the mechanisms by which NE cells influence prostate cancer growth and progression, especially after androgen ablation therapy, are poorly understood. To investigate the role of NE cells on prostate cancer growth, LNCaP xenograft tumors were implanted into nude mice. After the LNCaP tumors were established, the NE mouse prostate allograft (NE-10) was implanted on the opposite flank of these nude mice to test whether NE tumor-derived systemic factors can influence LNCaP growth. Mice bearing LNCaP tumors with or without NE allografts were castrated 2 weeks after NE tumor inoculation, and changes in LNCaP tumor growth rate and gene expression were investigated. After castration, LNCaP tumor growth decreased in mice bearing LNCaP tumors alone, and this was accompanied by a loss of nuclear androgen receptor (AR) localization. In contrast, in castrated mice bearing both LNCaP and NE-10 tumors, LNCaP tumors continued to grow, had increased levels of nuclear AR, and secreted prostate-specific antigen. Therefore, in the absence of testicular androgens, NE secretions were sufficient to maintain LNCaP cell growth and androgen-regulated gene expression in vivo. Furthermore, in vitro experiments showed that NE secretions combined with low levels of androgens activated the AR, an effect that was blocked by the antiandrogen bicalutamide. Because an increase in AR level has been reported to be sufficient to account for hormone refractory prostate cancers, the NE cell population ability to increase AR level/activity can be another mechanism that allows prostate cancer to escape androgen ablation therapy.

Androgens↗
PubMed1998

Delta opiate receptors account for the castration-induced unmasking of gonadotropin-releasing hormone binding sites in the rat pituitary.

Under control incubation conditions, gonadotropin-releasing hormone (GnRH) binds only a fraction of its receptors in rat-cultivated pituitary cells. Unmasking of the remaining receptors, which have been termed 'cryptic', requires drug- or peptide-induced protein kinase activation. Spontaneous masking however is not observed on pituitary cells sampled from castrated male rats, suggesting the presence of an intrinsic unmasking factor. Many endogenous factors could theoretically account for the effect. Here we attempted to identify the factor involved by taking advantage of their differential dependency upon second messengers and transduction cascades. Spontaneous unmasking of GnRH binding was found reversed by pertussis toxin (PTX), an inhibitor of alphai and alphao subunits of heterotrimeric G proteins, and by U73122, a phospholipase C (PLC) inhibitor. In contrast, desensitization of protein kinase C (PKC) or inhibition of tyrosine kinase by herbimycin were ineffective. Among endogenous pituitary factors able to unmask GnRH receptors in pituitary cells from normal male rats, as EGF, NPY or opiate peptides, only the latter were found to correspond to this transduction profile. In an attempt to characterize the pharmacology of opiate effects, naloxone (10 microM), a poorly selective opiate antagonist, restored masking of GnRH binding in cells from castrates. Only the delta antagonist naltrindole (1 microM) was able to mimick the action of naloxone. Conversely, when tested on cells from intact animals, morphine (10 microM), as well as dslet (1 microM) and met-ENK (10 nM), preferential delta agonists, but not dago and beta-endorphin or U50488 H and dynorphin, respectively micro and kappa agonists, were able to suppress masking. Among opioid peptides endogenous to the pituitary, only met-ENK was able to unmask cryptic receptors, an effect antagonized by naltrindole. We conclude that an opiate delta receptor subtype is endogenously activated in the pituitary of castrated male rats to prevent masking of GnRH binding.

Animals↗
PubMed2005

Testosterone reverses ethanol-induced deficit in spatial reference memory in castrated rats.

The present study was designed to evaluate the effects of ethanol, testosterone and combination of ethanol and testosterone, on spatial reference memory and beta-endorphin (beta-EN) levels in castrated rats. Male Sprague-Dawley rats (120-150 g) were used in this study, Animals were castrated and ethanol, testosterone or combination of the drugs were administered to rats at 09:00 h. The drugs were administered after a training period of 5 days and spatial reference memory was evaluated for 7 days using the Morris water maze. One hour after the last injection, animals were sacrificed, their brains removed and dissected into cortex, hypothalamus, hippocampus and midbrain. The beta-EN levels in these brain regions were determined by radioimmunoassay. The time to find the platform (latency period) was significantly increased in ethanol-treated rats, indicating that ethanol induces deficit in spatial reference memory. On the other hand, testosterone administration improved spatial reference memory by significantly decreasing the latency period. In addition, there was a significant decrease in latency period in the animals treated with combination of ethanol and testosterone. Results also indicate that administration of ethanol resulted in a significant increase in beta-EN levels in the hippocampus and in the cortex while concurrent administration with testosterone abolished this increase. These findings clearly indicate that administration of testosterone did not only improve memory but also abolished the spatial memory deficit induced by ethanol in castrated rats.

Animals↗
PubMed1985

Effects of castration and maturational age of male rats on the process of copper-stimulated release of luteinizing hormone releasing hormone from median eminence explants: evidence that androgens increase the affinity of the copper-interactive sites for copper.

We have previously shown that chelated copper stimulates the release of luteinizing hormone releasing hormone (LHRH) from explants of the median eminence area (MEA) incubated under in vitro conditions and that this stimulation involves a ligand-specific interaction. In this study, we addressed the question: do testicular steroids regulate the secretory response of LHRH neurons to copper? MEA, obtained from immature, mature, immature castrated and sham-operated rats, were incubated in the presence of various concentrations of copper for 15 min and then in the absence of copper for an additional period of 30 min. We noted that after a lag period of 5 min of incubation, the rate of LHRH release increased in a linear fashion for a period of 15 min. In addition, the rate of LHRH release as well as the rate at which LHRH release was accelerated were saturable functions of the concentration of copper. When incubation was carried out in the presence of a nonsaturating concentration of copper (50 microM), the fractional amount (percent of the total MEA content) of LHRH released from the MEA of castrated rats was significantly (p less than 0.001) lower than that from sham-operated rats; stimulated release being 0.9% and 1.4%, respectively. Similarly, copper-stimulated release from the MEA of immature rats was lower than that from the MEA of mature rats. However, when incubation was carried out in the presence of saturating concentrations of copper (100 or 200 microM), the percentage of stimulated release from the MEA of castrated rats was similar to that of sham-operated rats and significantly lower than that of mature and sham-operated rats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1987

In vivo activity of the LHRH pulse generator as determined with push-pull perfusion of the anterior pituitary gland of unrestrained intact and castrate male rats.

In the present article we report that in vivo LHRH output as measured at the anterior pituitary following castration significantly increased, due to larger and more frequent LHRH signals arriving to this gland. This contrasts with the decreased amplitude and overall mean LHRH release of castrate males bearing a push-pull cannula within the hypothalamus. These divergent results have generated a new thesis regarding the role of gonadal steroids upon the LHRH pulse generator. This thesis submits that following castration there is an increased frequency and decreased amplitude of the LHRH signal from discrete loci within the medial basal hypothalamus, but an increased synchrony of LHRH release throughout the entire hypothalamus, resulting in an increased frequency and amplitude of LHRH arriving at the anterior pituitary.

Animals↗