The effects of indomethacin on plasma LH levels in female and male deermice ( )

The purpose of this investigation was to determine (1) the approximate time of the preovulatory LH rise in cyclic deermice, (2) the effect of indomethacin administration on plasma LH levels during the expected preovulatory LH rise, and (3) the effect of indomethacin administration on plasma LH levels in castrated male deermice. The data indicate that the preovulatory LH rise occurred at about 2200 h on proestrus and that indomethacin pretreatment significantly reduced plasma LH levels during that time. In addition, indomethacin significantly reduced plasma LH levels in castrated male deermice. We conclude that plasma LH levels remain low throughout the estrous cycle with the exception of the preovulatory “surge”, that plasma LH levels in deermice are comparable to those reported for the rat, and that indomethacin pretreatment reduced plasma LH levels during periods when they were expected to be elevated (in castrated males and during the expected preovulatory LH rise in female deermice). The data are consistent with the hypothesis that the effect of indomethacin on plasma LH levels is due to an inhibitory effect on hypothalamic PG biosynthesis.     

Mediation by gonadal steroids of plasma beta-endorphin and LH in castrated female and male rats

Immunoreactive beta-endorphin (IR-BE) was significantly decreased and luteinizing hormone (LH) significantly increased in female rats castrated for four weeks. Forty eight hours after a single injection of estradiol benzoate (EB), IR-BE levels increased, and LH levels were reduced. On the afternoon following the administration of a second injection of EB given six hours earlier, IR-BE levels were reduced below control values, whereas LH levels were significantly elevated. There was no change in IR-BE levels during the remainder of that afternoon whereas LH levels decreased over time. Similar to female rats, IR-BE was diminished and LH increased in castrated male rats. IR-BE was increased significantly above those values observed in intact animals 24 hr after a single injection of TP and returned to control levels by 48 hr after administration of TP. Injection of TP reduced LH to levels observed prior to castration. These findings suggest that gonadal steroids exert a feedback on the release of IR-BE from the pituitary of female and male rats opposite to their feedback effect on the release of pituitary gonadotropins.     

Effects of a long-acting LHRH agonist preparation on plasma gonadotropin and prolactin levels in castrated male rats and on the release of prolactin from ectopic pituitaries

We have examined the effects of a single subcutaneous injection of an LHRH agonist, D-Trp-6-LHRH, in biodegradable microcapsules of poly(DL-lactide-co-glycolide) on plasma gonadotropin and prolactin (PRL) levels in castrated and in castrated-hypophysectomized-pituitary grafted (CAST-APX-GRAFT) male rats. The results were compared to the effects of daily injections of the same LHRH agonist dissolved in saline. In castrated rats, there were no significant alterations in plasma LH or PRL levels during the 10 days following the injection of LHRH agonist microcapsules, while FSH levels were generally reduced. In castrated males given daily injections of 6 micrograms of LHRH agonist in saline, plasma LH levels were significantly reduced while plasma PRL levels were not changed. In CAST-APX-GRAFT rats, both D-Trp-6-LHRH microcapsules and daily LHRH agonist injections appeared to increase plasma PRL levels. The pattern of changes in PRL release in both groups was similar, with levels on day 6 being significantly higher than those measured on days 1, 3 and 10 after onset of treatment. As expected, LH and FSH levels in these animals were extremely low. Immunoreactive D-Trp-6-LHRH was consistently detectable in the plasma of CAST-APX-GRAFT animals after microcapsule administration, whereas in animals given daily injections of this agonist in saline, its plasma concentrations were often below the detectability limit of the employed assay. These findings suggest that the LHRH agonist, D-Trp-6-LHRH, is capable of causing a short term stimulation of PRL release from ectopic pituitaries. Elevation of plasma LH levels is apparently not required for this effect.     

Gonadal steroid modulation of brain opioid systems

It is becoming increasingly clear that the effects of the opioids and their synthetic analogs on anterior pituitary function largely depend on the steroid milieu present in the animal at time of drug administration. However, it is still unclear whether gonadal steroids regulate the opioid-modulated mechanisms by affecting the number of opiate receptors in the brain. To further investigate these issues, the effects of opiate agonists and antagonists on LH, FSH and prolactin (Prl) secretion have been studied in: (a) normal and castrated male rats, and (b) normally cycling female rats. The binding characteristics of the brain subclass of mu opiate receptors have been analyzed in the same group of experimental animals; this type of receptors seems to be particularly involved in the control of gonadotropin and Prl release. When injected intraventricularly into normal male rats, morphine (200 micrograms/rat) induced in a significant elevation of serum LH levels at 10 and 20 min. In long-term castrated animals the administration of the drug significantly reduced LH secretion at 40 and 60 min after the injection, the inhibition lasted up to 180 min. Morphine, when given intraventricularly to normal males, induced a conspicuous and significant elevation of serum Prl levels at 10, 20, 40 and 60 min after treatment. However, when the drug was administered to castrated rats, it did not significantly affect Prl release at any time interval considered. Morphine intraventricular injections did not modify serum FSH levels either in normal or in castrated male rats. The concentration of mu opiate receptors was found to be similar when measured in the whole brain of normal and orchidectomized rats. In adult cycling female rats, s.c. injections of naloxone (2.5 mg/kg) stimulated LH release in every phase of the estrous cycle; the magnitude of the responses was highly variable, being particularly elevated at 16.00 h of the day of proestrous and at 10.00, 12.00 and 14.00 h of the day of estrous. Conversely, LH response to naloxone was totally obliterated at 18.00 and 20.00 h of the day of proestrous, when the preovulatory LH surge was found to occur. The concentration of brain opiate receptors of the mu type showed significant variations during the different phases of the estrous cycle, with higher levels at 12.00 h of the day of proestrous and at 18.00 h of the day of estrous.(ABSTRACT TRUNCATED AT 400 WORDS)     

Altered sexual development in male rats after oestrogen administration during the neonatal period.

Male rats given 250 mug oestradiol benzoate by subcutaneous injection on Day 4 of postnatal life showed a marked delay in the onset of the pubertal increase in the weight of the testes and seminal vesicles and in spermatogenesis but not a complete failure of sexual development. The increase in plasma testosterone concentration at puberty was also delayed in oestrogen-treated males but the eventual increase in seminal vesicle weight was closely related in time to the delayed increase in plasma testosterone concentration. Both plasma LH and FSH concentrations were reduced for about 10 days after oestrogen administration as compared to control values. After 22 days of age, plasma LH concentration did not differ significantly from the control values. The plasma FSH concentration of the oestrogen-treated males showed a delayed rise to values equal to or higher than those of controls of the same age. The delayed rise in plasma FSH concentration in the oestrogen treated males preceded the delayed rise in plasma testosterone in these animals. The decrease in plasma FSH concentration from the high prepubertal values to the lower values in adults occurred at different ages in the control and in oestrogen-treated rats but in both groups the decrease occurred as plasma testosterone levels were increasing and the first wave of spermatogenesis was reaching completion. The increase in plasma FSH concentration after castration was reduced in oestrogen-treated males during the period throughout which FSH levels in the intact animals were subnormal but the levels in oestrogen-treated males castrated after the delayed rise in FSH had occurred did not differ from control values. It is suggested that the delayed sexual maturation of male rats treated with high doses of oestrogen in the neonatal period is related principally to abnormalities in the secretion of FSH.     

Effects of acutely increased plasma testosterone concentrations on pulsatile luteinizing hormone secretion in the male rat

To assess the role of testosterone (T) in regulating the minute-to-minute release of pulsatile luteinizing hormone (LH) secretion in the adult male rat, we investigated the negative feedback of acute increases in plasma T concentrations on pulsatile LH secretion in acutely castrated male rats. At the time of castration, we implanted T-filled Silastic capsules, s.c., which maintained plasma T concentrations at approximately 1.8 ng/ml and suppressed LH pulses. On the next day, the capsules were removed; blood sampling (every 6 min) was started 8 h after implant removal, thereby allowing LH pulses to be reinitiated. Immediately following a control bleeding interval of 2 h, either T or vehicle alone was infused s.c., and blood sampling continued for another 4 h. In animals receiving vehicle alone, LH pulse frequency and mean LH levels increased over the 6 h bleeding period. The administration of 200 ng T/min caused a rapid rise in plasma T concentrations of about 4 ng/ml ("physiological") and prevented the increase in pulse frequency that occurred in the control group; it did not, however, reduce pulse frequency over the 4 h infusion period. When T was infused at the rate of 400 ng/ml, plasma T concentrations rose to approximately 18 ng/ml ("supraphysiological") and LH pulse frequency was significantly reduced, but not completely inhibited, during the last 2 h of the infusion. The pulse amplitude of luteinizing hormone did not change significantly in any of the groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modulation of luteinizing hormone(LH) release by clonidine and opioid peptides in castrated male rats

The effect of clonidine, a central alpha-adrenergic agonist, on the suppression of LH release induced by beta-endorphin or FK33-824, an endogenous opioid peptide or its synthetic analog, was investigated in castrated male rats, with or without pretreatment with reserpine. Pulsatile LH secretion was inhibited by intravenous injection of FK33-824 (400 micrograms/kg), or intraventricular injection of beta-endorphin (5 micrograms). Without pretreatment with reserpine, intraperitoneal administration of clonidine (1 mg/kg) failed to reverse the inhibition of LH release induced by these peptides. However, with pretreatment with reserpine (10 mg/kg), clonidine abolished the inhibitory effect on LH secretion induced by these peptides in castrated male rats. These data indicate that, unlike the results in ovariectomized, steroid-primed rats, pretreatment with reserpine allows the alpha-adrenergic system to act more peripherally than the opioid neuronal system in a neuronal network-regulating LH release in castrated male rats.     

Prostaglandin F2α (PGF2α) and prolactin secretion in rats

Plasma prolactin and F-prostaglandins (PGF) were measured in anesthetized male Sprague-Dawley rats before and at 15, 30, 45 and 60 minutes following i.v. injection of either PGF_2α (4 mg/kg), chlorpromazine, 1 mg/kg or chlorpromazine (1 mg/kg) after pretreatment with i.p. indomethacin (2 mg/kg). Following PGF_2α administration, plasma prolactin levels increased significantly only at 15 and 30 minutes in spite of extremely high PGF levels throughout 60 minutes. Besides the expected rise in plasma prolactin, chlorpromazine caused a transient but statistically significant increase in PGF. Indomethacin blocked the chlorpromazine-induced PGF rise but not prolactin increase. Animals stressed with ether anesthesia showed elevation of plasma prolactin, which was not blocked by indomethacin although PGF concentration fell. These results indicate that PGF_2α can stimulate prolactin release. This effect does not appear to be physiologic since very high PGF levels are required. Furthermore, blockade of prostaglandin synthesis by indomethacin does not prevent the release of prolactin in response to chlorpromazine or stress. Our findings do not support a possible role of PGFs as intermediaries in prolactin release. However, it is possible that PGFs may work through other mechanisms not investigated in our study.     

Effect of neonatal castration on the content of hypothalamic LHRH, pituitary LH and plasma LH in developing male rats.

The content of hypothalamic LHRH and concentration of LH in pituitary and plasma were measured on day 5, 7, 10, 14, 17, 22, 25, 30, 45, 52 and 60 in male rats which were bilaterally castrated on day 2. The levels of plasma LH were significantly higher in all the groups of castrated rats than in normal male rats of corresponding ages. The concentration of plasma LH did not rise progressively but showed day to day fluctuation apparently due to alteration of sexual differentiation of the hypothalamus. The concentration of pituitary LH was significantly lower in neonatally castrated rats compared to normal male rats except on days 17, 25 and 30. The content of hypothalamic LHRH declined initially following castration, but from day 17 onwards significantly higher levels of hypothalamic LHRH were maintained in neonatally castrated rats than in intact control. Initial decline in the content of hypothalamic LHRH may be because of stimulation of release of LHRH which exceeds maximal rate of synthesis and subsequent increase in the content of hypothalamic LHRH may be due to enhanced LHRH synthesis as a result of castration.     

Hypothalamic contents of LHRH and catecholamines during the ovulatory cycle of the hen (Gallus domesticus)

Concentrations of LHRH, dopamine, noradrenaline and adrenaline in the anterior hypothalamus-preoptic region (AH-POR) and posterior hypothalamus-median eminence (PH-me) were determined in hens killed at different times in relation to the first ovulation of a sequence. The occurrence of a preovulatory rise in plasma LH concentration 4-6 h before the expected time of ovulation was confirmed. This rise in plasma LH was accompanied by a significant (P less than 0.01) 50% reduction in the LHRH content of the AH-POR and PH-me while the subsequent fall in plasma LH was accompanied by a restoration of the LHRH content of both regions to their former levels. Although no significant fluctuations in the hypothalamic content of either dopamine, noradrenaline or adrenaline were detected during the ovulatory cycle, significant correlations between LHRH content and catecholamine content were observed in the AH-POR (P less than 0.05) and PH-me (P less than 0.01). Thus mean levels of each amine followed the same temporal pattern as LHRH content with minimum values being observed shortly before the peak of the preovulatory surge of LH. These findings support the conclusion that an enhanced secretion of LHRH from the median eminence, possibly associated with an increased activity of catecholaminergic neurones, is a prerequisite for the preovulatory release of LH in the hen.     

Prostaglandin F2alpha (PGF2alpha) and prolactin secretion in rats.

Plasma prolactin and F-prostaglandins (PGF) were measured anesthetized male Sprague-Dawley rats before and at 15, 30, 45 and 60 minutes following i.v. injection of either PGF2alpha (4 mg/kg), chlorpromazine, 1 mg/kg or chlorpormazine (1 mg/kg) after pretreatment with i.p. indomethacin (2 mg/kg). Following PGF2alpha administration, plasma prolactin levels increased significantly only at 15 and 30 minutes in spite of extremely high PGF levels throughout 60 minutes. Besides the expected rise in plasma prolactin, chlorpromazine caused a transient but statistically significant increase in PGF. Indomethacin blocked the chlorpormazine-induced PGF rise but not prolactin increase. Animals stressed with ether anesthesia showed elevation of plasma prolactin, which was not blocked by indomethacin although PGF concentration fell. Theese results indicate that PGF2alpha can stimulate prolactin release. This effect does not appear to be physiologic since very high PGF levels are required. Furthermore, blockade of prostaglandin synthesis by indomethacin does not prevent the release of prolactin in response to chlorpormazine or stress. Our findings do not support a possible role of PGFs as intermediaries in prolactin release. However, it is possible that PGFs may work through other mechanisms not investigated in our study.     

Effects of luteinizing hormone, progesterone, testosterone, estradiol and corticosterone on ovulation and luteinizing hormone release in hens treated with aminoglutethimide

Aminoglutethimide (AG), an inhibitor of steroidogenesis, was administered s.c. to 5 groups of laying hens at a dose of 200 mg AG/kg body weight 9 h before expected midsequence ovulation. This dose has previously been demonstrated to consistently block ovulation. The injection of AG was followed by s.c. injections of: Group 1, 1.0 mg progesterone; Group 2, 0.1 mg estradiol-17 beta; Group 3, 1.5 mg corticosterone, all at 6 h prior to expected ovulation; Group 4, 1.0 mg testosterone at both 8 h and 5 h before expected ovulation; and Group 5, 25 micrograms of ovine luteinizing hormone (LH) at 8 and 50 micrograms ovine LH at 6 h before expected ovulation. For each group, 4 control hens were injected with AG and the appropriate vehicle. Blood samples were taken at 1- or 2-h intervals from the time of AG injection to the expected time of ovulation. The hens were killed 4 h after expected ovulation and examined for the occurrence of ovulation. In all hens injected with vehicle, ovulation and the preovulatory surges of progesterone, testosterone, estradiol-17 beta and LH were inhibited. The plasma concentration of corticosterone was not reduced following an injection of AG. Four of 6 hens ovulated in response to injection of ovine LH, although neither endogenous LH nor progesterone were released. Thus, LH appears to play a direct role in follicular rupture and extrusion of the ovum. The administration of progesterone induced a significant and prolonged rise in LH, restoring AG-blocked ovulation in all hens treated (n = 6). Injections of testosterone restored LH release in all hens and ovulation in 2 of 7 hens treated. Three of 7 hens ovulated in response to the corticosterone injection. A preovulatory rise in LH was not observed, indicating that corticosterone may exert its ovulation-inducing effect directly on the mature follicle. Estradiol-17 beta did not restore LH release or ovulation in any of the hens treated with AG.     

Plasma LH, FSH, testosterone, prolactin and androstenedione in male white-tailed deer after ACTH and dexamethasone administration

1. In order to investigate the role of the adrenocortical system in the regulation of plasma levels of reproductive hormones, adult male white-tailed deer (five intact and one castrated) from a captive herd were sedated with xylazine and ketamine and then challenged with various doses of ACTH with and without dexamethasone (DX) pretreatment. 2. Plasma levels of LH, testosterone (T), FSH, prolactin (PRL) and androstenedione (A) were determined by RIA in serial samples taken from the jugular vein. 3. An increase of A levels detected after ACTH in both intact and castrated deer indicated stimulation of secretion of adrenal androgens by ACTH. 4. No effect on FSH and PRL levels was observed in either group. 5. A significant decline of LH and T observed in various treatments could not be attributed to ACTH or DX administration. It is speculated that the decrease may be caused by anaesthetics which alleviate the stress induced in deer by the pre-immobilization activities.     

Feedback regulation of gonadotropic hormone secretion in neonatal pigs

The effect of castration and of administration of charcoal-treated porcine follicular fluid (pFF) containing inhibin-like activity on plasma concentration of gonadotropic hormones was studied in neonatal pigs. Plasma follicle-stimulating hormone (FSH) concentration averaged 25.1 +/- 1.5 ng/ml (mean +/- SEM) in 1-wk-old females and gradually declined to 20.2 +/- 0.7 ng/ml 6 wk later. Ovariectomy did not significantly influence plasma FSH concentration. In males, concentration averaged 8.0 +/- 0.7 ng/ml before castration but rose significantly within 2 days after castration. Injection of luteinizing hormone-releasing hormone (LHRH) did not influence plasma FSH concentrations in intact males, but did in females and in 7-wk-old males castrated at 1 wk. Plasma luteinizing hormone (LH) concentrations in 1-wk-old females (2.2 +/- 0.4 ng/ml) gradually declined and were not influenced by castration. Concentrations of plasma LH in 1-wk-old male piglets (2.8 +/- 0.7 ng/ml) were not significantly influenced by castration within 2 days but were significantly higher 6 wk later. LHRH induced a significant rise in plasma LH concentrations in all animals. Injection of pFF resulted in a decline of plasma FSH concentrations in intact and castrated males and in intact females, but did not influence plasma LH concentrations. These data demonstrate a sex-specific difference in the control of plasma FSH, but not in plasma LH concentration in the neonatal pig. Plasma FSH concentrations, but not plasma LH concentrations, are suppressed by testicular hormones in 1-wk-old piglets. Plasma FSH concentrations can be suppressed in both neonatal male and female pigs by injections of pFF.     

Direct effect of prolactin, induced by TRH injection, on ovarian oestradiol secretion in the ewe

The effect of sustained high plasma levels of prolactin, induced by repeated 2-h i.v. injections of thyrotrophin-releasing hormone (TRH; 20 micrograms), on ovarian oestradiol secretion and plasma levels of LH and FSH was investigated during the preovulatory period in the ewe. Plasma levels of progesterone declined at the same rate after prostaglandin-induced luteal regression in control and TRH-treated ewes. However, TRH treatment resulted in a significant increase in plasma levels of LH and FSH compared to controls from 12 h after luteal regression until 5 to 6 h before the start of the preovulatory surge of LH. In spite of this, and a similar increase in pulse frequency of LH in control and TRH-treated ewes, ovarian oestradiol secretion was significantly suppressed in TRH-treated ewes compared to that in control ewes. The preovulatory surge of LH and FSH, the second FSH peak and subsequent luteal function in terms of plasma levels of progesterone were not significantly different between control and TRH-treated ewes. These results show that TRH treatment, presumably by maintaining elevated plasma levels of prolactin, results in suppression of oestradiol secretion by a direct effect on the ovary in the ewe.     

Effects of hyperprolactinemia on the control of luteinizing hormone and follicle-stimulating hormone secretion in the male rat

Experiments were conducted to determine the effects of acute hyperprolactinemia (hyperPRL) on the control of luteinizing hormone and follicle-stimulating hormone secretion in male rats. Exposure to elevated levels of prolactin from the time of castration (1 mg ovine prolactin 2 X daily) greatly attenuated the post-castration rise in LH observed 3 days after castration. By 7 days after castration, LH concentrations in the prolactin-treated animals approached the levels observed in control animals. HyperPRL had no effect on the postcastration rise in FSH. Pituitary responsiveness to gonadotropin hormone-releasing hormone (GnRH), as assessed by LH responses to an i.v. bolus of 25 ng GnRH, was only minimally effected by hperPRL at 3 and 7 days postcastration. LH responses were similar at all time points after GnRH in control and prolactin-treated animals, except for the peak LH responses, which were significantly smaller in the prolactin-treated animals. The effects of hyperPRL were examined further by exposing hemipituitaries in vitro from male rats to 6-min pulses of GnRH (5 ng/ml) every 30 min for 4 h. HyperPRL had no effect on basal LH release in vitro, on GnRH-stimulated LH release, or on pituitary LH concentrations in hemipituitaries from animals that were intact, 3 days postcastration, or 7 days postcastration. However, net GnRH-stimulated release of FSH was significantly higher by pituitaries from hyperprolactinemic, castrated males. To assess indirectly the effects of hyperPRL on GnRH release, males were subjected to electrical stimulation of the arcuate nucleus/median eminence (ARC/ME) 3 days postcastration. The presence of elevated levels of prolactin not only suppressed basal LH secretion but reduced the LH responses to electrical stimulation by 50% when compared to the LH responses in control castrated males. These results suggest that acute hyperPRL suppresses LH secretion but not FSH secretion. Although pituitary responsiveness is somewhat attenuated in hyperprolactinemic males, as assessed in vivo, it is normal when pituitaries are exposed to adequate amounts of GnRH in vitro. Thus, the effects of hyperPRL on pituitary responsiveness appear to be minimal, especially if the pituitary is exposed to an adequate GnRH stimulus. The suppression of basal LH secretion in vivo most likely reflects inadequate endogenous GnRH secretion. The greatly reduced LH responses after electrical stimulation in hyperprolactinemic males exposed to prolactin suggest further that hyperPRL suppresses GnRH secretion.     

Effects of Adrenocorticotropin Treatment on Estrogen,Luteinizing Hormone,and Progesterone Secretion in the Female Rhesus Monkey

Adrenocorticotropin (ACTH) was administered to female rhesus monkeys in order to determine the effects of adrenal axis activation on the endocrine events occurring during the menstrual cycle. ACTH injected twice daily during the follicular period and through the time of expected ovulation was found to prevent the rise of estrogens during the follicular phase. In addition, the ACTH administration also blocked the preovulatory surge of LH, prevented the luteal rise of progesterone, and extended the length of the menstrual cycle.     

A 'window of time' during which testosterone determines the opiatergic control of LH release in the adult male rat

Male rats castrated before puberty (when 26 days of age) showed a progressively decreasing susceptibility to the inhibitory effects of morphine (5 mg/kg) upon LH secretion for up to 28 days after gonadectomy (approximately 100%, 40% and 10% inhibition at 5, 12 and 28 days after castration), but thereafter morphine again caused approximately 50% reduction in serum LH values; the minimum inhibition found at 28 days after castration (age 54 days) occurred at the time at which male rats normally reach puberty. When rats were castrated at 59 days of age, morphine maximally suppressed serum LH concentrations (to less than 70%) 2 and 5 days after castration, but had no effect thereafter. In prepubertal castrates, testosterone replacement between Days 26 and 50 of life resulted in responses to morphine similar to those found in rats castrated after puberty, i.e. serum LH levels were not reduced. Morphine significantly reduced LH levels in prepubertal castrates given testosterone after 60 days of age. Treatment with morphine consistently elevated serum prolactin concentrations (greater than 100%) in castrated rats of all ages, regardless of the time elapsed after gonadectomy. These results indicate a transient fall in the inhibitory opioidergic tone upon LH secretion as the normal age of puberty approaches, that the ability of opiates to alter LH release in adulthood may depend upon testicular steroids secreted during the peripubertal period, and that the LH responses do not reflect general changes in the neuroendocrine response to opiates after castration since the prolactin response to morphine remains intact in rats castrated before and after puberty.     

Effect of immobilization stress on the gonadotropic function of the hypophysis in male hamadryas baboons (Papio hamadryas)

The plasma levels of luteinizing hormone (LH) and testosterone were studied in intact and castrated male baboons exposed to 2- and 10-hour periods of immobilization. Presented data have shown that immobilization stress induced a marked decrease in LH concentration both in intact and castrated monkeys. Changes in LH concentration positively correlated with plasma levels of testosterone only during the experimental procedures. During three days after immobilization there was a sharp dissociation in the dynamics of testosterone levels remained low and LH returned to normal values. We can suggest that it is not absolute LH level that is responsible for the changes in testosterone secretion during the immobilization stress.     

Effects of gonadotropin-releasing hormone administration on the pituitary-gonadal axis in male and female dogs before and after gonadectomy

GnRH-stimulation tests were performed in 14 female and 14 male client-owned dogs of several breeds, before and 4 to 5 mo after gonadectomy. The aim of the study was to obtain more insight into the pituitary-gonadal axis in intact and neutered dogs and to establish reference values. Basal plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations were increased significantly after gonadectomy in both bitches and male dogs. In both males and females ranges of the basal plasma FSH concentrations, before and after gonadectomy, did not overlap as opposed to the overlap in ranges of the basal plasma LH concentrations. Before gonadectomy basal plasma LH concentrations were lower and basal plasma FSH concentrations were higher in bitches than in male dogs. After gonadectomy these basal values did not differ significantly. GnRH administration before gonadectomy resulted in an increase in plasma LH and FSH concentrations in both genders. GnRH administration after gonadectomy produced an increase only in plasma LH concentrations in both genders, and a just significant increase in plasma FSH in castrated male dogs. GnRH administration before gonadectomy resulted in a significant increase in plasma testosterone concentration in both genders. In males ranges of basal and GnRH-stimulated plasma testosterone concentrations before and after gonadectomy did not overlap. Basal plasma estradiol concentrations were significantly higher in intact males than in castrated males and their ranges did not overlap. The basal estradiol concentrations in bitches before and after ovariectomy were not significantly different. At 120 min after GnRH administration, ranges of plasma estradiol concentration of intact and ovariectomized bitches no longer overlapped. In conclusion, basal plasma FSH concentration appears to be more reliable than basal plasma LH concentration for verification of neuter status in both male and female dogs. The basal plasma testosterone concentration appears to be reliable for verification of neuter status in male dogs. The plasma estradiol concentration at 120 min after GnRH administration can be used to discriminate between bitches with and without functional ovarian tissue.