Ivermectin impairs sexual behavior in sexually naïve, but not sexually experienced male rats

Ivermectin (IVM) is an antiparasitic drug, widely used in domestic animals. In mammals, IVM act as a GABA agonist. This neurotransmitter has an important role in the regulation of sexual behavior. Thus, this study sought to investigate the effects of various medically relevant doses IVM on the sexual behavior of male rats. In particular, we also wished to examine if previous sexual experience modulated responses to IVM. In the first experiment, the sexual behavior of inexperienced male rats was analyzed after they received 0.2, 0.6, 1.0 or 2.0 mg/kg IVM, 15 min prior to behavioral testing. In the second experiment, the effects of four previous sexual experiences on IVM treated rats (1.0 or 2.0 mg/kg, 15 min prior to the 5th session) were assessed. The standard therapeutic dose (0.2 mg/kg) did not impair the sexual behavior of inexperienced male rats. At a more concentrated dose (0.6 mg/kg), which is still within the therapeutic range, the appetitive phase of sexual behavior of inexperienced male rats was impaired. Likewise, 1.0 mg/kg impaired the appetitive phase. Previous sexual experience blocked almost entirely this sexual impairment, suggesting that previous sexual experience exerts a positive effect in attenuating the sexual impairment produced by IVM treatment. Therefore, the standard therapeutic dose of IVM can be used without producing side effects on sexual behavior. Use of more concentrated therapeutic doses is not recommended during reproductive periods, unless the animals have had previous sexual experience.     

Fourth ventricular alloxan injection suppresses pulsatile luteinizing hormone release in female rats

Previous studies have suggested the presence of a glucose-sensing mechanism in the hindbrain that appears to regulate reproductive function as well as feeding behavior. The ependymocytes lining the ventricular wall of the hindbrain showed immunoreactivities to pancreatic glucokinase (GK), a key enzyme for glucose sensing in pancreatic B cells. Our goal in the present study was to test whether the GK-immunopositive ependymocytes in the wall of the fourth cerebroventricle (4V) play a role in regulating gonadal activity. Our approach was to determine the effect of injecting alloxan, a GK inhibitor, into the 4V on pulsatile luteinizing hormone (LH) secretion. Estrogen-primed ovariectomized rats received an injection of alloxan (10 or 20 microg/animal) into the 4V and blood samples were collected every 6 min for 3 h for measurement of blood LH, corticosterone and glucose levels. Pulsatile LH secretion was suppressed after alloxan injection and all pulse parameters were significantly (P<0.05) inhibited by 20 microg alloxan. Plasma corticosterone levels were increased significantly (P<0.05) by 20 microg alloxan, suggesting that LH pulse suppression by alloxan may be at least partly mediated by activation of the hypothalamo-pituitary-adrenal axis. The present results suggest that acute suppression of GK activity in the hindbrain inhibits pulsatile LH secretion in female rats, and supports the idea that GK-immunopositive ependymocytes may sense glucose levels in the cerebrospinal fluid and play a role in regulation of LH secretion.     

Effects of sequential or group exposure to unrestrained estrual females on expression of sexual behavior in sexually experienced beef bulls

We tested the hypothesis that expression of sexual behavior in bulls is affected by the manner in which they are exposed to unrestrained, sexually receptive females. Twelve Angus bulls were used in a crossover design involving two treatments, each tested four times for a total of eight tests for each bull. Sexual interactions were quantified for each of four, 30-min periods under the following treatments: 1) exposure to each of four estrual females in sequence (SEQ); or 2) exposure to four estrual females as a group (GRP). Bulls were blocked into three testing groups, the order of which was stratified across eight test days. The order in which bulls were tested on a particular day had no effect on bulls' expression of mount interactions, or flehmen responses, suggesting that each group of bulls had similar sexual motivation at the beginning of each test. However, the bull testing order x treatment x time interaction influenced mounting interval (P = 0.08), copulation frequency (P <0.05), and copulation success ratio (P <0.05). When bulls were in GRP and tested first on test days, more (P <0.05) copulations were distributed to the first three females encountered compared with either the fourth female (P <0.05) or to each of the other females in SEQ (P <0.05). During later tests, other bulls in GRP were not able to copulate as frequently (P <0.05) with each female, displayed lower (P <0.05) copulation success ratios, and were allowed copulations by fewer (P <0.05) females during each 30-min test. When bulls were in SEQ, they displayed similar numbers of copulations regardless of the order in which they were tested, and had stable mounting intervals; however, copulation success ratio decreased (P <0.05) more rapidly during subsequent tests. Flehmen responses were initially displayed more frequently (P <0.05) when bulls were in GRP, but this effect diminished during subsequent 30-min tests. In conclusion, exposure of bulls to GRP induced greater sexual responsiveness than SEQ; however, this effect was due to enhanced sexual activity during the early stages of sexual encounters and with females that were not recently mated. Interestingly, bulls seem to repeatedly copulate with each individual female until, apparently, female sexual receptivity became attenuated. Thereafter, recently mated females allowed fewer episodes of repeated copulations, but they did not completely cease copulating with novel bulls.     

Central estrogen action sites involved in prepubertal restraint of pulsatile luteinizing hormone release in female rats

The present study aimed to determine estrogen feedback action sites to mediate prepubertal restraint of gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) release in female rats. Wistar-Imamichi strain rats were ovariectomized (OVX) and received a local estradiol-17β (estradiol) or cholesterol microimplant in several brain areas, such as the medial preoptic area (mPOA), paraventricular nucleus, ventromedial nucleus and arcuate nucleus (ARC), at 20 or 35 days of age. Six days after receiving the estradiol microimplant, animals were bled to detect LH pulses at 26 or 41 days of age, representing the pre- or postpubertal period, respectively. Estradiol microimplants in the mPOA or ARC, but not in other brain regions, suppressed LH pulses in prepubertal OVX rats. Apparent LH pulses were found in the postpubertal period in all animals bearing estradiol or cholesterol implants. It is unlikely that pubertal changes in responsiveness to estrogen are due to a change in estrogen receptor (ER) expression, because the number of ERα-immunoreactive cells and mRNA levels of Esr1, Esr2 and Gpr30 in the mPOA and ARC were comparable between the pre- and postpubertal periods. In addition, kisspeptin or GnRH injection overrode estradiol-dependent prepubertal LH suppression, suggesting that estrogen inhibits the kisspeptin-GnRH cascade during the prepubertal period. Thus, estrogen-responsive neurons located in the mPOA and ARC may play key roles in estrogen-dependent prepubertal restraint of GnRH/LH secretion in female rats.     

Increased testosterone secretion in bulls treated with a luteinizing hormone releasing hormone (LHRH) agonist requires endogenous LH but not LHRH

The requirement for endogenous LHRH and LH action in the maintenance of elevated plasma concentrations of testosterone in bulls receiving the LHRH agonist deslorelin was examined. In Experiment 1, bulls were either (i) left untreated (control); (ii) implanted with deslorelin; (iii) actively immunized against LHRH; or (iv) implanted with deslorelin and immunized against LHRH. Experiment 2 was of similar design to Experiment 1, except that bulls were immunized against LH in place of LHRH. In Experiment 1, plasma LH declined in bulls immunized against LHRH, but not in the bulls immunized against LHRH and implanted with deslorelin. Also in Experiment 1, plasma testosterone declined in bulls immunized against LHRH but was elevated in bulls treated with deslorelin and bulls treated with deslorelin and immunized against LHRH. In Experiment 2, bulls immunized against LH and treated with deslorelin had plasma concentrations of testosterone similar to controls, whereas bulls treated only with deslorelin had elevated plasma testosterone. It was concluded from these experiments that endogenous LHRH action was not required for increased steroidogenic activity in bulls treated with a LHRH agonist. However, circulating LH was necessary for increased plasma testosterone in bulls implanted with deslorelin. LH is therefore involved in mediating the response of bulls to treatment with deslorelin, either by acting directly at the testes or through a permissive role that allows a direct action of deslorelin at the testes.     

Effect of cortisol on luteinizing hormone release during sexual behavior in the boar.

The effect of inhibiting the rise in cortisol concentrations that occurs at copulation upon luteinizing hormone release was studied in seven adult boars. Plasma samples were collected for assay of luteinizing hormone, testosterone and cortisol on a control day and before, during and after exposure to an estrous sow. The area under the curve was used to evaluate hormone production and treatment effects were evaluated by a paired Student's t-test. The 11 beta-hydroxylase inhibitor, metyrapone, was used to suppress glucocorticoid hormone production. Cortisol concentrations increased significantly (p less than 0.05) after breeding compared to values on the control day while treatment with metyrapone prior to breeding prevented the cortisol increase (p greater than 0.05). Although luteinizing hormone production increased significantly after copulation in both breeding experiments, metyrapone pretreatment resulted in a reduction of luteinizing hormone secretion (p less than 0.05). Testosterone production was also reduced in boars pretreated with metyrapone. The results suggest that the increased levels of cortisol occurring at copulation may enhance luteinizing hormone release in boars.     

Effects of zeranol on reproduction in beef bulls: luteinizing hormone, follicle-stimulating hormone, and testosterone secretion in response to gonadotropin-releasing hormone and human chorionic gonadotropin

Effects of zeranol on the maturation of the adenohypophyseal-gonadal axis were studied in beef bulls. Calves were implanted with 36 mg of zeranol at 3-month intervals from birth through 6 months of age (group 2, n = 10) or were not treated (control group 1, n = 10). After 9 months, group-2 calves were given implants of 36 mg of zeranol at 3-month intervals through 18 months of age (group 2B, n = 5) or were not reimplanted (group 2A, n = 5). Areas under the curves outlined by concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone for 6 hours after the administration of 100 micrograms of gonadotropin-releasing hormone (GnRH) were calculated. Gonadotropin-releasing hormone was administered at 3-month intervals from 1.5 through 19.5 months of age. Areas under the curves for concentrations of testosterone for 4 hours after the administration of 10,000 IU of human chorionic gonadotropin (HCG) at 4.5, 7.5, and 10.5 months or 1,000 IU at 13.5 and 16.5 months of age also were calculated. The amount of FSH released was greater (P less than 0.05) for group-2 than for group-1 calves at 4.5 and 7.5 months of age. The amount of FSH released in groups 2A and 2B tended (P less than 0.10) to be greater than that for group 1. Significant differences between groups 2A and 2B were not observed. The amount of LH released at 7.5 months of age was less for groups 1 and 2 than that at earlier ages, and the decrease was greater (P less than 0.05) for group 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of cortisol, luteinizing hormone, and testosterone responses to a defined stressor in sexually inactive rams and sexually active female-oriented and male-oriented rams

The objective of this study was to determine whether the effect of restraint stress on cortisol, LH, and testosterone varied among sexually inactive and sexually active female- and male-oriented rams, to allow differentiation among ram classes. Restraint stress or no stress was imposed on sexually inactive (n = 7) and sexually active female- (n = 17) and male-oriented (n = 6) rams in a 2 x 3 factorial arrangement. Rams were assigned to restraint or control within each classification. Rams were habituated to wearing halters and being tethered in separate pens, permitting visual, vocal, and olfactory contact with adjacent rams for 7 d before treatment. After 1 d of habituation, rams were fitted with jugular catheters that were checked twice daily for patency. For restraint stress, rams were laid on their side with their legs tied for 1 h. For no stress, rams were tethered with halters and leads, but their legs were not tied. On the treatment day, blood was collected at 30-min intervals for 3 h followed by 15-min intervals for 1 h before restraint, during 1-h restraint, and for 1 h after liberation from restraint. Then blood was collected at 30-min intervals for an additional 2 h. Blood was collected from controls at similar intervals. Control rams were isolated from stressed rams. Cortisol, LH, and testosterone were measured using RIA. Mixed model analyses with repeated measures were used on transformed data. Average prestress data were used as a covariate. Cortisol increased (P < 0.01) within 15 min after restraint and remained increased until 1.5 h after liberation from 1-h of restraint stress. In contrast, in controls cortisol remained unchanged at 5 ng/ mL. Cortisol did not differ over time among ram classes, and the treatment x ram class x time interaction was not significant. For LH and testosterone, the ram class x time interactions appeared to compromise the ability to identify differences in these hormones, indicating that they were not good endocrine candidates for methods of classifying rams. In conclusion, restraint stress increased cortisol in sexually inactive and sexually active female- and male-oriented rams alike, thus not providing a method to differentiate among ram classes.     

Inability to predict sexual and aggressive behaviors by plasma concentrations of testosterone and luteinizing hormone in Hereford bulls

The relationships between sexual and aggressive behaviors and levels of plasma testosterone and luteinizing hormone (LH) were examined in Hereford bulls at 18 and 24 mo of age. Concentrations of hormones in bulls during periods of sexual rest (13 blood samples collected from each animal during a 24-h period) were compared with individual differences in sexual and aggressive behaviors when exposed to restrained females, either individually or in groups. Nearly all correlation coefficients were low and nonsignificant. It was concluded that individual differences in sexual performance and aggressive behavior cannot be predicted based on circulating levels of testosterone and LH in bulls during periods of sexual rest.     

N-methyl-d,l-aspartate stimulates growth hormone and prolactin but inhibits luteinizing hormone secretion in the pig.

The effects of n-methyl-d,l-aspartate (NMA), a neuroexcitatory amino acid agonist, on luteinizing hormone (LH), prolactin (PRL) and growth hormone (GH) secretion in gilts treated with ovarian steroids was studied. Mature gilts which had displayed one or more estrous cycles of 18 to 22 d were ovariectomized and assigned to one of three treatments administered i.m.: corn oil vehicle (V; n = 6); 10 micrograms estradiol-17 b/kg BW given 33 hr before NMA (E; n = 6); .85 mg progesterone/kg BW given twice daily for 6 d prior to NMA (P4; n = 6). Blood was collected via jugular cannulae every 15 min for 6 hr. Pigs received 10 mg NMA/kg BW i.v. 2 hr after blood collection began and a combined synthetic [Ala15]-h GH releasing factor (1-29)-NH2 (GRF; 1 micrograms/kg BW) and gonadotropin releasing hormone (GnRH; .2 micrograms/kg BW) challenge given i.v. 3 hr after NMA. NMA did not alter LH secretion in E gilts. However, NMA decreased (P < .02) serum LH concentrations in V and P4 gilts. Serum LH concentrations increased (P < .01) after GnRH in all gilts. NMA did not alter PRL secretion in P4 pigs, but increased (P < .01) serum PRL concentrations in V and E animals. Treatment with NMA increased (P < .01) GH secretion in all animals while the GRF challenge increased (P < .01) serum GH concentrations in all animals except in V treated pigs. NMA increased (P < .05) cortisol secretion in all treatment groups. These results indicate that NMA inhibits LH secretion and is a secretagogue of PRL, GH and cortisol secretion with ovarian steroids modulating the LH and PRL response to NMA.     

Effects of natural mating stimuli on serum luteinizing hormone, testosterone and estradiol-17 beta in yearling beef bulls

The objective of this study was to determine the effect of natural mating stimuli on serum concentrations of LH, testosterone (T) and estradiol-17 beta (E2) in beef bulls. Twenty sexually experienced, yearling beef bulls were bled every 15 min during a 9-h period, 4 h before and 5 h after exposure to estrual females. For exposure, each bull was placed individually in an isolated pen with two restrained estrual heifers for 10 min or until one service was achieved. Timing and number of all behavioral events, including flehmen responses, abortive mounts and services, were recorded for each bull by two independent observers. Of the 20 bulls, 9 bulls mounted and were removed immediately after achieving a service, 8 bulls mounted without achieving a service and 3 bulls exhibited no interest during exposure. Twelve bulls achieved fewer than three and eight bulls achieved three or more flehmen responses during exposure. Postexposure responses in LH, T and E2 were not consistently correlated with number of mounts or presence or absence of a service. However, postexposure LH and T, but not E2, responses were highly correlated with number of flehmen responses achieved (r = .40 to .66; P = .08 to .001). In bulls that achieved three or more flehmen responses, serum LH increased within 30 min after exposure (P = .02) and serum T was increased dramatically within 1 h after exposure (P less than .01), compared with preexposure hormone concentrations, regardless of the number of mounts and regardless of the presence or absence of a service. Natural mating stimuli had no effect on serum E2, and mounting activity alone and mounting that culminated in a service did not necessarily result in increased LH or T in beef bulls. However, number of flehmen responses achieved during exposure to females dramatically influenced postexposure serum LH and T concentrations in beef bulls.     

Progesterone concentration,estradiol pretreatment,and dose of gonadotropin-releasing hormone affect gonadotropin-releasing hormone-mediated luteinizing hormone release in beef heifers

We examined whether progesterone (P₄)-induced suppression of LH release in cattle can be overcome by an increased dose of exogenous gonadotropin-releasing hormone (GnRH) or pretreatment with estradiol (E₂). In Experiment 1, postpubertal Angus-cross heifers (N = 32) had their 2 largest ovarian follicles ablated 5 d after ovulation. Concurrently, these heifers were all given a once-used, intravaginal P₄-releasing insert (CIDR), and they were randomly assigned to be given either prostaglandin F_2α (Low-P₄) or no treatment (High-P₄) at follicle ablation, and 12 h later. Six days after emergence of a new follicular wave, half of the heifers in each group (n = 8) were given either 100 or 200 μg of GnRH i.m. Plasma luteinizing hormone (LH) concentrations were higher in the Low- vs High-P₄ groups, and in heifers given 200 vs 100 μg of GnRH (mean ± SEM 15.4 ± 2.2 vs 9.1 ± 1.2, and 14.8 ± 2.1 vs 9.8 ± 1.4 ng/mL, respectively; P ≤ 0.01). Ovulation rate was higher (P = 0.002) in the Low-P₄ group (15/16) than in the High-P₄ group (6/16), but it was not affected by GnRH dose (P = 0.4). In Experiment 2, heifers (n = 22) were treated similarly, except that 5.5 d after wave emergence, half of the heifers in each group were further allocated to be given either 0.25 mg estradiol benzoate i.m. or no treatment, and 8 h later, all heifers were given 100 μg GnRH i.m. Both groups treated with E₂ (Low- and High-P₄) and the Low-P₄ group without E₂ had higher peak plasma LH concentrations compared to the group with high P₄ without E₂ (12.6 ± 1.8, 10.4 ± 1.8, 8.7 ± 1.3, and 3.9 ± 1.2 ng/mL, respectively; (P < 0.04)). However, E₂ pretreatment did not increase ovulation rates in response to GnRH (P = 0.6). In summary, the hypotheses that higher doses of GnRH will be more efficacious in inducing LH release and that exogenous E₂ will increase LH release following treatment with GnRH were supported, but neither significantly increased ovulation rate.     

Elicitation of release of luteinizing hormone by N-methyl-d,l-aspartic acid during three paradigms of suppressed secretion of luteinizing hormone in the female pig.

Two experiments were conducted to determine the minimal effective dose during lactation and site of action of N-methyl-d,l-aspartic acid (NMA) for elicitation of release of luteinizing hormone (LH) in female pigs. In the first experiment, three doses of NMA were given to lactating primiparous sows in which endogenous LH was suppressed by suckling of litters. In the second experiment, ovariectomized gilts were pretreated with estradiol benzoate or porcine antisera against GnRH to suppress LH and then given NMA to determine if it elicited secretion of LH directly at the anterior pituitary or through release of GnRH. In experiment 1, 3 lactating sows (17 +/- 1.5 d postpartum) were each given three doses of NMA (1.5, 3.0 and 5.0 mg/kg body weight [BW]; IV) on 3 consecutive days in a Latin Square design. Blood samples were collected every 10 min from -1 to 1 hr from injection of NMA. NMA at 1.5 and 3.0 mg/kg did not affect (p greater than .5) secretion of LH; however, 5 mg NMA/kg elicited a 114% increase (p less than .001) in circulating levels of LH during 1 hr after treatment. In experiment 2, 8 ovariectomized gilts were given either estradiol benzoate (EB; 10 micrograms/kg BW; IM n = 4) to suppress release of GnRH or porcine antiserum against GnRH (GnRH-Ab; titer 1:8,000; 1 ml/kg BW; IV; n = 4) to neutralize endogenous GnRH. Gilts infused with GnRH-Ab were given a second dose of antiserum 24 hr after the first. Gilts were then given NMA (10 mg/kg BW; IV) 33 hr after EB or initial GnRH-Ab. Blood samples were drawn every 6 hr from -12 to 24 hr from EB or GnRH-Ab treatments, and every 10 min from -2 to 2 hr from NMA. Serum LH declined (p less than .001) after EB (from 1.87 +/- .2 ng/ml at 12 hr before EB to 0.46 +/- .02 ng/ml during 24 hr after EB) and GnRH-Ab (from 1.97 +/- .1 to 0.59 +/- .02 ng/ml). In gilts treated with EB, the area under the curve (AUC) for the LH response (ng.ml-1.min) 1 hr after NMA (38.7 +/- 3) was significantly greater (p less than .01) than the 1 hr prior to NMA (21.3 +/- 1.5). Treatment with NMA had no effect (p greater than .5) on secretion of LH in gilts infused with GnRH-Ab.(ABSTRACT TRUNCATED AT 400 WORDS)     

Seasonal differences in the parameters of luteinizing hormone release to exogenous gonadotropin releasing hormone in prepubertal Holstein heifers in Sapporo

Stress due to summer heat has adverse effects on reproduction in Holstein dairy cattle. Summer suppression of reproduction of Holsteins can pose an important economic problem, even in Hokkaido prefecture located in the northern region of Japan. Hokkaido is one of the most important dairy farming areas of Japan. This study is an attempt to clarify the seasonal differences in the parameters of luteinizing hormone (LH) response to exogenous gonadotropin releasing hormone (GnRH) in Sapporo, Hokkaido, Japan. A total of 12 prepubertal heifers received an injection with GnRH analogue intramuscularly in either May (n=4, May group), July (n=4, July group), or November (n=4, November group), and serial blood samples were collected to analyze the parameters of the LH response curve after GnRH injection. The parameters were as follows: the basal LH concentration, peak LH concentration, duration from the time of GnRH injection to the time of the peak LH concentration, and area under the LH response curve (AUC). There were no significant differences in the basal and peak LH concentrations or the AUC among the three groups. The July group reached the LH peak significantly (P<0.05) faster than the May group, but there was no significant difference with the November group. Therefore, the results of the present study do not demonstrate an effect of summer heat on the LH response to the exogenous GnRH in Holstein heifers.     

Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits

The intramuscular administration of adrenocorticotrophic hormone (ACTH) to calves, in either a short-acting form (cosyntrophin) or a longer-acting form (ACTHAR Gel), failed to induce any alteration in circulating fibrinogen or fibronectin values, despite marked elevations in plasma cortisol concentrations. With the longer-acting ACTH, plasma cortisol was elevated for at least 12 h following treatment and induced the expected physiological response of an elevation in blood glucose. In contrast, both forms of ACTH induced marked increases (p<0.01) in plasma fibrinogen and fibronectin when administered to rabbits. The elevation in the circulating levels of these proteins was first observed 24 h after ACTH administration, by which time plasma corticosteroid values had returned to pre-treatment values. With both ACTH preparations the increases in the circulating levels of these proteins were sustained for at least 96 h. The results suggest that, in cattle, the well-recognized increases in plasma fibrinogen values following stress are not associated with the concomitant increase in plasma cortisol. Further, the results clearly illustrate the marked species differences in the response of acute-phase reactant proteins to elevated glucocorticoids.     

Ingestion of starch-rich meals after exercise increases glucose kinetics but fails to enhance muscle glycogen replenishment in horses

Fatiguing exercise substantially decreases muscle glycogen concentration in horses, impairing athletic performance in subsequent exercise bouts. Our objective was to determine the effect of ingestion of starch-rich meals after exercise on whole body glucose kinetics and muscle glycogen replenishment. In a randomized, cross-over study seven horses with exercise-induced muscle glycogen depletion were either not fed for 8 h, fed half of the daily energy requirements ( approximately 15 Mcal DE) as hay, or fed an isocaloric amount of corn 15 min and 4 h after exercise. Starch-rich meals fed after exercise, when compared to feed withholding, resulted in mild to moderate hyperglycemia (5.7+/-0.3 vs. 4.7+/-0.3 mM, P<0.01) and hyperinsulinemia (79.9+/-9.3 vs. 39.0+/-1.9 pM, P<0.001), 3-fold greater whole body glucose kinetics (15.5+/-1.4 vs. 5.3+/-0.4 micromol kg(-1)min(-1), P<0.05), but these only minimally enhanced muscle glycogen replenishment (171+/-19 vs. 170+/-56 and 260+/-45 vs. 294+/-29 mmol/kg dry weight immediately and 24 h after exercise, P>0.05). It is concluded that after substantial exercise-induced muscle glycogen depletion, feeding status only minimally affects net muscle glycogen concentrations after exercise, despite marked differences in soluble carbohydrate ingestion and availability of glucose to skeletal muscle.     

Comparison of the ability of the three endogenous GnRHs to stimulate release of follicle-stimulating hormone and luteinizing hormone in chickens

It is well established that GnRH can stimulate the release of LH and FSH in mammals. Two GnRHs have been found in the chicken hypothalamus, cGnRH-I and -II. There is controversy as to whether either peptide can stimulate release of FSH in birds. The present studies compared the ability of cGnRH-I and -II to stimulate the release of FSH and LH in chickens. Lamprey (l) GnRH-III may be a specific-releasing factor for FSH, as it selectively stimulates FSH release in rodents and cattle, and has been detected in the hypothalamus of rodents, sparrows and chickens. Therefore, the ability of lGnRH-III to stimulate LH and FSH release was also examined. In our first experiment, the effects of cGnRH-I and -II were studied using 17-week prepubertal females. Intravenous injection of cGnRH-II at 1 and 10 microg/kg BW significantly increased LH secretion more than did cGnRH-I. Neither peptide significantly increased plasma FSH levels. In our second study, we administered cGnRH-I, -II or lGnRH-III to mature males maintained on a short photoperiod. cGnRH-II was again more potent than cGnRH-I in stimulating LH release, while lGnRH-III produced a modest LH rise. No GnRH peptide provided specific or potent stimulus to FSH secretion, although the high dose of cGnRH-II modestly enhanced FSH levels in the adult male (P < 0.05). Our results are not consistent with the view that lGnRH-III is a specific FSH-releasing hormone across multiple classes of vertebrates. We conclude that the mechanism by which independent release of FSH occurs in chickens remains unresolved.