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Male Reproductive Tract |
Department of Biological Sciences,3 Macquarie University, North Ryde, New South Wales 2109, Australia
Peptech Animal Health Pty. Limited,4 North Ryde, New South Wales 2109, Australia
Department of Zoology,5 University of Melbourne, Victoria 3010, Australia
AgResearch,6 Wallaceville Animal Research Centre, Upper Hutt, New Zealand
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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gonadotropin-releasing hormone, luteinizing hormone, pituitary, testis, testosterone
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The endocrine response to continuous GnRH agonist treatment can be characterized by two phases, the acute phase, which can last for several days, and the chronic phase [18]. During the acute phase, there is an initial hyperstimulation of LH and FSH, followed by an increase in testosterone. This is followed by a chronic phase in which LH and testosterone production may be inhibited, unchanged, or elevated, depending on the species. Despite this variation between species, pituitary insensitivity to a GnRH challenge test has been demonstrated in male sheep [2], rhesus monkeys [6, 7], marmosets [12], and cattle [14, 19]. These findings suggest that downregulation and desensitization of pituitary gonadotropes may be a common phenomenon in males of all species during GnRH agonist treatment regardless of the long-term effects on basal LH and testosterone secretion [14].
Members of the kangaroo and wallaby family (Macropodidae) are held in large numbers in zoos and wildlife parks throughout the world. Under these circumstances, there is often a need to control population size. Reversible fertility control techniques that are applicable to both sexes and are without negative side-effects may prove to be valuable population management tools. This will be especially so when the maintenance of genetic diversity is paramount. Control of male aggressive behavior, especially in large kangaroo species, can become an issue in captive situations. If GnRH agonist treatment is effective at suppressing testosterone concentrations in male wallabies, this may be a promising way of controlling problem behavior in captivity, as the expression of male-type sexual behavior in the tammar wallaby appears to be determined by the activating effects of testosterone during adulthood [20]. The use of GnRH agonists to control aggressive sociosexual behavior has also been suggested for free-living male Hawaiian monk seals [21] and captive wild carnivore species [22].
Male tammar wallabies become sexually mature by 25 mo of age, as demonstrated by a fully functional hypothalamic-pituitary-gonadal axis [23]. At the beginning of the breeding season in January, testosterone and LH concentrations are significantly elevated [24] coincident with increases in the weight of accessory reproductive organs [25] in preparation for the highly synchronous period of mating that occurs in wild populations. No seasonal changes have been observed in the weight of the testes or epididymides, and spermatogenesis occurs all year [25, 26].
This study examines whether treatment with slow-release implants containing the GnRH agonist deslorelin suppresses the pituitary-testicular axis in the male tammar wallaby. The primary aims were to investigate the long-term effects of three dosages of deslorelin on basal plasma concentrations of LH and testosterone, on testis size, and on general health using body weight as an indicator. Multiple dosages were tested because variable effects have been reported in some species in relation to the dose of agonist [4, 5]. Secondary aims were to characterize the acute LH and testosterone response to deslorelin within the first 24 h of administration and to ascertain the degree of pituitary desensitization [27] after prolonged deslorelin treatment by measuring the response to exogenous GnRH.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The tammar wallabies used in this experiment were captured on Kangaroo Island in August 1999. For the duration of the experiment, from December 1999 until September 2000, they were held in bachelor groups at Macquarie University in grassed outdoor yards adjacent to groups of cycling females. The animals were fed specially formulated kangaroo cereal pellets (Gordon Specialty Stock Feed) with water available ad libitum. All males selected for this experiment were sexually mature, as judged by body and testes size, and had an average weight of 6.95 ± 0.19 kg (mean ± SEM). The Macquarie University Animal Ethics Committee approved all experimental work (approval number 99009), and animal handling and husbandry were conducted in accordance with National Health and Medical Research Council of Australia guidelines [28].
GnRH Agonist Implant
The GnRH agonist deslorelin (D-Trp6-Pro9-des-gly10-GnRH ethylamide) was formulated into implants containing 5 mg of deslorelin (Peptech Animal Health Pty. Limited, North Ryde, NSW, Australia) as previously described [5]. In a real-time dissolution system, the release of deslorelin was >1 µg/day for periods of approximately 1 yr [5]. The in vivo release rate in tammar wallabies is not known. The dimensions of a 5-mg deslorelin implant were 2.3 mm in width and 12.5 mm in length. Implants were placed subcutaneously between the shoulder blades using a commercial implanting device, sterilized by e-beam radiation. The injection site was then sealed with a veterinary tissue adhesive (Vetbond; 3M Animal Care Products, St Paul, MN). Dosages of >5 mg were administered using a syringe that was preloaded with two implants (10 mg of deslorelin) prior to the sterilization process. The 20-mg dose was achieved by administering two 10-mg doses.
Experimental Design
Male tammars were assigned to one of four groups (n = 6/group) using a completely random design and received one of the following treatments: control, placebo implant; low dose, one deslorelin implant (5 mg); medium dose, two deslorelin implants (10 mg); high dose, four deslorelin implants (20 mg). The approximate dosages of deslorelin received over the period of release (total dose/mean weight) were low dose, 0.71 mg; medium dose, 1.40 mg; high dose, 2.75 mg deslorelin/kg.
Three baseline samples were collected 14 days apart before deslorelin administration in early December 1999. On the day of treatment (20 January 2000), a blood sample was collected immediately before implant insertion (0 h) and then at 2, 4, 6, 8, and 24 h after implant insertion (acute sampling period). Blood samples were then collected once every 7 d for 56 d and then once every 14 d for the next 112 d following implant administration.
At the time of blood collection, the width and length (excluding the epididymis) of the left testis was measured using vernier callipers, and the animal was weighed. Evaluation of the testis measurement data indicated that there had not been a decline in testis size over time for any dosage, as would be expected if chronic exposure to deslorelin were suppressing gonadal activity [2, 4, 5, 29]. It was therefore decided to perform a GnRH challenge test to determine if the pituitary had become desensitized to exogenous GnRH as a result of deslorelin treatment. The GnRH challenge was performed on all animals over a period of 12 days in late July and early August 2000, between 186 and 197 days after deslorelin administration.
Blood Sampling
During regular sampling, blood was collected between 0730 and 1000 h from the lateral tail vein using a 21-gauge winged infusion set and a 5- ml syringe. Blood was transferred immediately to heparinized blood collection tubes (Vacuette, lithium heparin; Greiner Labortechnik, Kremsmuenster, Austria) and held on ice until centrifugation. The plasma was separated and stored in two aliquots at –20°C until assayed to determine the concentrations of testosterone and LH.
Acute blood sampling For the duration of the acute sampling period (24 h), animals were held in hessian sacks suspended from a frame in an air-conditioned room. Blood samples (3 ml) were collected alternately from left and right lateral tail veins at 0, 2, 4, 6, 8, and 24 h relative to implant administration.
GnRH challenge Animals were placed in a hessian sack with their tail protruding from a hole at the base of the sack and a 22-gauge-indwelling catheter (Terumo) fitted in the lateral tail vein. The catheter was kept patent with heparinized saline (100 IU/ml in sterile 0.9% NaCl) between each sample. Blood samples (2 ml) were collected at –20, –10, 0, 10, 20, 30, 40, 60 and 90 min relative to injection of GnRH (2 µg/kg i.v. in sterile 0.9% saline; Fertagyl; Intervet [Aust] Pty. Ltd., Castle Hill, NSW, Australia).
Hormone Assays
LH assay Plasma LH concentrations were determined using the method of Moore et al. [30] validated for the tammar wallaby. The assay used antiserum raised against ovine LH in the rabbit (Wa-R oLH; AgResearch, Wallaceville, New Zealand) and purified possum LH as the standard (AgResearch). All samples from individual animals were run in the same assay to reduce variability. The assay sensitivity was 0.1 ng possum LH/ ml plasma. Dilutions of tammar wallaby pituitary homogenates and plasma pools from castrated wallabies were found to be parallel to the possum LH standard curve. The interassay coefficients of variation calculated for three quality control pools containing 0.34 ± 0.04 ng/ml, 1.18 ± 0.11 ng/ ml, and 6.7 ± 0.71 ng/ml (mean ± SD) were 13.2%, 9.7%, and 10.6%, respectively. The intraassay coefficients of variation for the same pools were 7.6%, 5.3%, and 9.2%, respectively.
Testosterone assay Plasma testosterone concentrations were determined using the method of Williamson et al. [23]. Plasma samples were extracted using a mixture of n-hexane:toluene (2:1). The assay used antiserum no. 6050 (provided by Dr. R.I. Cox, Bioquest Ltd., North Ryde, NSW, Australia) raised in sheep against testosterone-3-carboxymethyloxine conjugated to bovine serum albumin. All samples from individual animals were run in the same assay to reduce variability. The efficiency of a double extraction of 200 µl of plasma by 2 ml n-hexane:toluene (2:1) was 91% and the assay sensitivity was 64 pg testosterone/ml plasma. The intraassay coefficients of variation calculated for two quality control pools containing 2.68 ± 0.08 ng/ml and 5.88 ± 0.21 ng/ml (mean ± SD) were 3.0% and 3.7%, respectively. The interassay coefficients of variation for three pools containing 0.79 ± 0.06 ng/ml, 2.04 ± 0.17 ng/ml, and 5.69 ± 0.44 ng/ml were 7.2%, 8.2%, and 7.7%, respectively.
Statistical Analyses
Data for testosterone and LH concentration, testis size, and animal weight over time were analyzed by analysis of variance (ANOVA) procedures using the general linear model (GLM) repeated measures procedure of SPSS (SPSS Inc., Chicago, IL), the model being y = treatment, time, treatment x time, with time as the repeated subject. Multiple comparisons of group means were conducted using the Tukey honestly significant difference (HSD) test by means of the GLM Post Hoc Multiple Comparisons function of SPSS. The relative effects of treatment group and weight on testosterone concentrations after treatment were evaluated using the multivariate repeated measures analysis procedure of Systat. Criteria for determining whether an individual had a positive response to the GnRH challenge were based on the pattern of response and the magnitude of the peak relative to the starting concentrations. A positive response was recorded if the peak value was greater than two times the standard deviation of the three pre-GnRH samples (–20, –10, and 0 min) and if the peak occurred between 20 and 30 min or 90 min after GnRH injection for LH and testosterone, respectively, based on the pattern of response in control animals. Comparisons of the mean testosterone and LH concentration for each group during the GnRH challenge and acute sampling period were analyzed by ANOVA procedures using the GLM repeated measures procedure of SPSS. Data at single time points were analyzed using paired- sample t-tests for comparisons within groups or two-sample t-tests for comparisons between groups. Where necessary, data were transformed to log10 before analysis to attain homogeneity of variance. However, results are reported as untransformed arithmetic means ± SEM.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Mean weights of animals in each group at the start of the experiment were 6.31 ± 0.32 kg (control), 7.05 ± 0.38 kg (low), 7.15 ± 0.27 kg (medium), and 7.27 ± 0.46 kg (high). Although the average weight of control animals was less than treated animals, there was no significant difference between the groups (P > 0.05). Throughout the course of deslorelin treatment, control tammars remained lighter, on average, than treated animals (Fig. 1), but this difference was not significant (P > 0.05). Similarly, there was no significant treatment x time interaction (P > 0.05).
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Testis Size
There was a significant difference in mean testis length (Fig. 2a) and testis width (Fig. 2b) measurements between the groups (P < 0.05 for both) throughout the course of deslorelin treatment. The significance was predominantly accounted for by differences between the control group and the three treatment groups, with the control group having significantly smaller testes, in terms of width and length, than all three treatment groups from the start until the completion of deslorelin treatment (Tukey HSD multiple comparisons, P < 0.05 for control versus low, medium, and high doses for testis width and length). There was no significant treatment x time interaction (P > 0.05) for testis length or width, indicating that any changes over time were not significantly different between all four groups. Testis length and width did not change significantly within any of the groups between the beginning and end of the sampling period (P > 0.05 for all groups).
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Plasma LH and Testosterone
Acute response to deslorelin After deslorelin administration, plasma LH concentrations were significantly elevated within 2 h for all treatment groups (P < 0.001; control, 0.27 ± 0.09; low, 13.49 ± 1.31; medium, 13.31 ± 2.17; high, 10.08 ± 1.19 ng/ml). Concentrations continued to rise until they peaked between 4 and 6 h after implant insertion (low, 19.86 ± 1.74 ng/ml at 4 h; medium, 16.55 ± 1.87 ng/ml at 4 h; high, 16.21 ± 3.67 ng/ml at 6 h). By 24 h, LH concentrations were still significantly higher than control animals (P < 0.001) but had declined significantly from peak concentrations (Fig. 3a). By the time of the next sample, 7 d after deslorelin administration, LH concentrations had returned to pretreatment levels. There was no significant difference between the acute plasma LH responses to the three different doses of deslorelin (Tukey HSD multiple comparisons P > 0.05).
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Plasma testosterone concentrations had also significantly increased by 2 h after deslorelin administration in all three treatment groups (P < 0.0001; control, 1.84 ± 0.62; low, 9.25 ± 0.53; medium, 9.65 ± 1.03; high, 10.27 ± 0.78 ng/ ml). At this time, testosterone concentrations reached a plateau and remained elevated until 24 h after deslorelin administration, with no evidence of a decline within this period (Fig. 3b). By the time of the next sample (Day 7), testosterone concentrations had returned to pretreatment levels. There was no significant difference in the testosterone response to the three different doses of deslorelin (Tukey HSD multiple comparisons, P > 0.05). Throughout the acute sampling period, testosterone concentrations declined significantly in control animals from a starting concentration of 3.72 ± 0.96 to 0.97 ± 0.52 ng/ml at 24 h (P < 0.01).
Long-term response to deslorelin Before the onset of treatment, there were no differences in the mean plasma concentrations of LH or testosterone between the four groups (P > 0.05), although there was a significant increase in both hormones over the pretreatment period coincident with the initiation of the breeding season in all four groups (Figs. 4 and 5). Repeated measures analysis of variance from Day 0 to Day 190 of deslorelin treatment indicated that there were no significant detectable differences in LH concentrations between the four groups (P > 0.05; Fig. 4), but the concentrations measured were close to the sensitivity of the assay.
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Deslorelin administration occurred at a time when testosterone concentrations were already elevated at the start of the breeding season for all groups (Fig. 5). Analysis from Day 0 to Day 190 showed that there was a significant treatment (P < 0.05), time (P < 0.001), and treatment x time (P = 0.001) interaction. Following deslorelin administration, testosterone concentrations declined from the early breeding season peak but remained at significantly higher concentrations in treated animals than control animals, which exhibited a decline in testosterone concentrations as the breeding season progressed (control, 1.33 ± 0.11; low, 2.55 ± 0.10; medium, 3.30 ± 0.20; high, 3.13 ± 0.25 ng/ ml).
Correlation Between Weight, Testis Size, and Testosterone
Random assignment of animals into groups resulted in a bias toward larger animals in the treatment groups compared with the control group in terms of both body weight and testis size. Multivariate repeated measures analysis postdeslorelin treatment showed that there was a significant effect of weight on testosterone concentrations (P < 0.005), but no significant effect was attributed to treatment group (P > 0.05). In addition, linear regressions of the pretreatment testosterone versus weight and testes size data for all animals showed there was a significant positive relationship between testosterone concentration and both weight (y = 1.12x – 3.89, R2 = 0.31, P = 0.005) and testis width (y = 3.76x – 6.31, R2 = 0.21, P = 0.02), but there was substantial variation between animals. The strongest relationship was between testis length and testosterone (y = 5.51x – 16.52, R2 = 0.57, P < 0.0001).
GnRH challenge Starting concentrations of LH were not significantly different between the four groups (P > 0.05; control, 0.16 ± 0.03; low, 0.16 ± 0.03; medium, 0.22 ± 0.04; high, 0.17 ± 0.03 ng/ml). Following GnRH administration to control animals, LH concentrations increased within 10 min and peaked at a concentration of 2.92 ± 0.83 ng/ml at the 20-min sample (Fig. 6a). Mean LH concentrations in treated animals showed a similar pattern of response, but the magnitude of the peak was reduced compared with control animals (control, 2.92 ± 0.83; low, 1.99 ± 1.00; medium, 0.46 ± 0.20; high, 0.70 ± 0.30 ng/ml). Repeated measures analysis of variance showed that time (P < 0.001), treatment (P < 0.05), and treatment x time (P < 0.001) were all significant, as can be seen by the change in LH concentrations over time and the variability in the magnitude of the response between the three groups in Figure 6a.
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Testosterone concentrations were higher in treated groups than the control group immediately before GnRH administration, although the difference was not significant (P > 0.05; control, 1.12 ± 0.39; low, 1.73 ± 0.28; medium, 2.91 ± 0.98; high, 2.19 ± 0.45 ng/ml). Control animals responded to GnRH with a gradual increase in testosterone that peaked at 6.85 ± 1.42 ng/ml (611% of Time 0 basal values) at the 90-min interval (Fig. 6b). The response of treated animals varied between the three groups. Low-dose animals responded with a gradual increase in testosterone, similar to the control animals but lower in magnitude (4.46 ± 1.12 ng/ml, 258% of Time 0 value). The high-dose group showed very little response (3.59 ± 1.21 ng/ml, 164% of Time 0 value), while the medium-dose group appeared to have no testosterone response to the GnRH challenge (2.96 ± 1.25 ng/ml, 102% of Time 0 value). Repeated measures analysis from Time 0 min indicated that time and treatment x time were significant (P < 0.001), as can be seen by the changes in testosterone over time and the marked differences in responses between the groups. However, there was no significant difference between the treatment groups (P > 0.05), reflecting the high variability of responses within each group and the variable starting concentrations.
Some of the variability within groups is due to the variable responses of individual animals. Within the treated groups, some animals showed a response to the GnRH challenge and other animals had no response, i.e., they had a desensitized pituitary. The number of animals that had a positive response to the GnRH challenge varied between the groups, as did the magnitude of their response (Table 1). All six control animals had a positive LH and testosterone response to the GnRH challenge. Four animals (of six) in the low-dose group had a positive response, and the magnitude of this response was only slightly lower than control animals for both LH and testosterone. A small LH response was induced in just one medium-dose animal, but testosterone did not increase in any animals. The one responsive animal also had a slight rise in testosterone but did not meet the response criteria, primarily because of the high variability in testosterone concentrations during the pre-GnRH sampling period. Two high-dose animals had positive LH and testosterone responses to the challenge. The magnitude of their LH response was lower than control animals but testosterone concentrations were very similar.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The acute response of male tammars to deslorelin administration demonstrates that deslorelin is biologically active in the tammar wallaby. There was no difference in the acute LH and testosterone responses to administration of different dosages of deslorelin, suggesting that the pituitary and testes were maximally stimulated by even the lowest dose. During the acute sampling period, there was a significant decline in the concentration of testosterone in control animals. A similar response to frequent blood sampling over extended periods was demonstrated by Lincoln [33] in a range of macropodid marsupials. In his study, Lincoln attributed the progressive decline of testosterone to the stress of restraint and frequent blood sampling. These results show that this effect must be mediated at the hypothalamic-pituitary level.
Following the acute changes within the first 24 h, continued long-term deslorelin treatment subsequently had no detectable effect on basal LH concentrations, but testosterone concentrations were significantly higher in treated animals compared with control animals over all dosages. Deslorelin administration occurred at a time when testosterone concentrations were already elevated at the beginning of the breeding season [24]. Following deslorelin administration, testosterone concentrations remained elevated in treated animals, while they declined to lower concentrations in control animals as the breeding season progressed. However, treated animals weighed more on average than control animals and had significantly larger testes both before and during deslorelin treatment. This was an artefact of the random assignment of animals to experimental groups. The higher testosterone concentrations appeared to be correlated with the larger size of the treated animals rather than a treatment effect. Nonetheless, the male tammar wallaby did not show any evidence of suppression of the pituitary-testicular axis during chronic GnRH agonist treatment.
Similar atypical responses have been demonstrated in marmoset monkeys, in which there is no significant decline in testosterone [12, 13]; and in red deer stags [11] and bulls [14, 16], where GnRH agonist treatment results in an elevation of testosterone concentrations. The mechanisms of action that result in maintenance of basal LH while testosterone secretion is either unchanged or increased in the bull, deer, tammar, and marmoset are not clearly understood. Much research has been devoted to elucidating these mechanisms in the bull [34]. The maintenance of basal LH in bulls is associated with reduced pituitary contents of LH and LHß-subunit mRNA [35], abolition of LH pulsatility, and a reduction in the number of pituitary GnRH receptors [15]. It is possible that basal LH secretion is maintained by a gradual depletion of the pituitary LH stores. However, this is unlikely to explain the maintenance of basal LH secretion for such long periods, e.g., 190 and 120 days in the tammar (this study) and bull [14], respectively.
Despite the apparent insensitivity to the contraceptive effects of deslorelin, most treated males did not respond to a GnRH challenge. Therefore, the apparent maintenance of basal LH concentrations masks an underlying pituitary desensitization. The positive response of some treated males to the GnRH challenge may be the result of an earlier recovery from desensitization rather than an outright resistance to the effects at the level of the pituitary. Studies using the same deslorelin implants in dogs and cats have demonstrated that there is considerable individual variation in the duration of contraceptive effects [5, 36]. This appears to be the case for tammars, with 7/17 animals responsive to a GnRH challenge approximately 190 days after the initiation of treatment. In addition, the animals that received the lowest dose (5 mg) appeared to recover more rapidly than animals receiving either of the two higher doses (10 or 20 mg). This was demonstrated by a greater number of animals responding to the GnRH challenge. Similarly, when bulls were given a GnRH challenge on Day 120 of deslorelin treatment, those with four or eight implants failed to respond, while those that received one implant showed a small LH response that was accompanied by a significant rise in testosterone [14]. Therefore, there may be a relationship between the dose of deslorelin and the duration of effects in a range of species.
An alternative explanation for the positive response to the GnRH challenge is that there may be some animals that are resistant to the desensitizing effects of chronic GnRH agonist treatment and as such are nonresponders. Concurrent studies on female tammars have demonstrated that there are some females that appear to maintain the ability to come into estrus during deslorelin treatment [37]. Therefore, the available data suggest that there is a proportion of the population that may be resistant to GnRH agonist-induced pituitary desensitization. It is plausible that a similar level of nonresponse is present in male tammars and this would be reflected in a continued response to a GnRH challenge during agonist treatment.
The lack of a decline in testosterone in the present study is unlikely to be a result of insufficient dose or an inefficient delivery system. The dosages administered to tammars were equivalent to doses given to bulls [14, 16] and those effective at suppressing testicular function in dogs [5]. In the numerous studies that have been conducted on bulls, testicular suppression cannot be induced at any dose [14]. In the present study, deslorelin was administered in slow- release implants, which is one of the most effective ways of providing constant exposure to the agonist. In addition, deslorelin is an extremely potent agonist [38], much more potent than others, such as buserelin, that have been shown to successfully downregulate the pituitary-testicular axis in a range of other species. It is unlikely that the differential responses in males of different species, such as tammars, bulls, red deer, and marmosets are related to dosages or methods of administration. It is more likely that, at the testicular level, these species have different regulatory mechanisms for control of testosterone secretion [17].
In summary, the male tammar appears to be resistant to the contraceptive effects of chronic GnRH agonist treatment over a wide range of dosages. Male tammars can maintain tonic LH secretion at a level adequate to maintain testicular function despite the loss of ability to respond to a GnRH challenge with a surge of LH. This supports previous suggestions that pituitary desensitization appears to be a common phenomenon in all species despite the apparent differential effects of agonist treatment on basal levels of testosterone and LH [16]. This inhibition of the LH surge system, while tonic LH secretion appears unaffected, may explain why fertility is impaired in the female tammar [37] but does not appear to be impaired in the male tammar (this study). In terms of management objectives, deslorelin implants would not be an effective contraceptive agent or behavioral modifier for male tammar wallabies. Whether the tammar is a valid model for other macropodid marsupials in this respect requires further research. The close evolutionary relationship between these species suggests that it could be.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Correspondence. FAX: 61 2 9850 9686; cherbert{at}rna.bio.mq.edu.au
Received: 11 November 2003.
First decision: 7 December 2003.
Accepted: 7 February 2004.
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REFERENCES |
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This article has been cited by other articles:
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  C.A. Herbert, D.C. Eckery, T.E. Trigg, and D.W. Cooper Chronic Treatment of Male Tammar Wallabies with Deslorelin Implants During Pouch Life: Effects on Development, Puberty, and Reproduction in Adulthood Biol Reprod, June 1, 2007; 76(6): 1054 - 1061. [Abstract] [Full Text] [PDF]
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 C A Herbert, T E Trigg, M B Renfree, G Shaw, D C Eckery, and D W Cooper Long-term effects of deslorelin implants on reproduction in the female tammar wallaby (Macropus eugenii) Reproduction, March 1, 2005; 129(3): 361 - 369. [Abstract] [Full Text] [PDF]
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, n = 6), low (•, n = 6), medium (
, n = 5), and high dose (
, n = 6) tammars after administration of deslorelin implants (
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)
, Deslorelin administered; 
, GnRH challenge; ——, breeding season
, deslorelin administered; 
, GnRH challenge; ——, breeding season