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a The University of Texas at Austin, Marine Science Institute, Port Aransas, Texas 78373
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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-dihydrotestosterone, a nonaromatizable androgen, was ineffective. Pretreatment of fish with an aromatase inhibitor, 1,4,6-androstatrien-3,17-dione, 2 days before the administration of testosterone implants, completely blocked the negative effect of testosterone on LHRHa-induced GTH II secretion in males, but only partially restored it in females. This suggests that the negative feedback of testosterone in males is primarily mediated by its conversion to estradiol at the level of the hypothalamus and/or pituitary gland, while in females the androgen may also exert a direct inhibitory effect on GTH II secretion, probably mediated via an androgen receptor. In addition, estradiol and testosterone exerted positive effects on basal and LHRHa-induced GTH II secretion during the early-recrudescence phase of the gonadal cycle. The steroids switched to a negative effect on LHRHa-induced GTH II secretion once the fish had fully developed gonads, possibly as a mechanism that prevents a precocious surge in GTH II secretion and final gamete maturation until gametogenesis is complete and the environmental conditions are appropriate for spawning.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Negative effects of gonadal steroids on gonadotropin secretion have been demonstrated in a variety of teleost species by using gonadectomy and steroid replacement protocols. Removal of gonads increases gonadotropin II (GTH II) secretion in the goldfish (Carassius auratus), African catfish (Clarias gariepinus), Indian catfish (Heteropneustes fossilis), and some salmonids during later stages of gonadal recrudescence [7–11]. This effect can be reversed by treatment with testosterone and/or estradiol [7, 8, 10]. In addition, castration in African catfish increases the gonadotropin response to buserelin, a GnRH agonist [12]. These effects have been interpreted as evidence for negative feedback regulation of gonadotropin secretion by gonadal steroids [7–12]. However, a negative feedback of testosterone or estradiol on LHRH analog (LHRHa)-induced gonadotropin secretion similar to that observed in tetrapods [2–6] has not been demonstrated in teleosts. In addition to negative effects, there is evidence that gonadal steroids also exert a positive influence on gonadotropin production in juvenile salmonids, European eel (Anguilla anguilla), black carp (Mylopharyngodon piceus), and striped bass (Morone saxatilis) [13–16]. Furthermore, long-term implants of testosterone in juvenile rainbow trout [16], and testosterone in combination with LHRHa in juvenile striped bass [17], exert a positive influence on circulating GTH II levels. Interestingly, a positive effect of the gonads on basal GTH II secretion has recently been shown in adult male Atlantic salmon throughout gonadal recrudescence [18]. Moreover, estradiol potentiates LHRHa-induced GTH II secretion without altering basal hormone secretion in adult goldfish throughout the gonadal cycle except during the late-recrudescence phase [19, 20]. Thus, gonadal stage is a major factor that modulates GTH II synthesis and release and the gonadotropin response to stimulation by LHRHa in teleosts.
The negative effect of testosterone on basal GTH II secretion in African catfish and its potentiating effect on LHRHa-induced GTH II secretion in goldfish appear to be mediated by aromatization of the androgen to estrogens at the level of brain and/or pituitary gland [8,19]. This is not surprising since many of the effects of testosterone in the vertebrate brain are mediated by its conversion to estradiol by aromatase [21, 22], and high concentrations of the enzyme have been detected in the teleostean brain and pituitary [23]. Aromatase activity in the brain and pituitary is regulated by gonadal steroids in mammals and fish and is concentrated in the areas of hypothalamus that have high concentrations of steroid receptors [1, 24–26]. Thus, there is both a physiological and morphological basis for possible interactions between steroid receptors and aromatase activity in the steroid feedback regulation of gonadotropin secretion.
Amino acid and monoamine neurotransmitters like gamma-aminobutyric acid (GABA), serotonin (5-hydroxytryptamine, 5-HT), and dopamine act as intermediaries in some of the steroid effects on gonadotropin secretion in mammals and fishes [1, 6, 27, 28]. We have previously shown that GABA and 5-HT are involved in the control of GTH II secretion in the Atlantic croaker (Micropogonias undulatus), and that the effects of these neurotransmitters depend on the stage of gonadal development [29–31]. The inhibitory dopaminergic mechanism controlling gonadotropin secretion in several teleost species is absent in Atlantic croaker and other perciform fishes, similar to the situation in mammalian species such as the rat [17, 32, 33]. Thus, Atlantic croaker is an interesting vertebrate model for investigating the neuroendocrine control of GTH II secretion. Gonadal steroids most likely modulate at least some of the neurotransmitter influences on GTH II secretion in croaker; therefore, it is important to investigate how these steroids influence GTH II secretion during its gonadal cycle.
In the present study, we investigated the roles of testosterone, 5-dihydrotestosterone, and estradiol in the control of basal and LHRHa-induced GTH II secretion, and pituitary GTH II content, in gonad-intact and gonadectomized spermiating male, and late-recrudescing and fully recrudesced female, Atlantic croaker. Lack of a significant effect in the experiments with 5-dihydrotestosterone, a nonaromatizable androgen, prompted further examination of whether the negative effect of testosterone on LHRHa-induced GTH II secretion observed in either sex is mediated by its aromatization to estradiol. Implants of an aromatase inhibitor, 1,4,6-androstatrien-3,17-dione, 2 days before testosterone implants, were employed to inhibit endogenous aromatase activity and prevent conversion of exogenous testosterone to estradiol. In addition, experiments using multiple injections of testosterone and estradiol were conducted to determine whether the two steroids influence basal and/or LHRHa-induced GTH II secretion, and pituitary GTH II content, during the early-recrudescence phase of the gonadal cycle.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Young-of-the-year Atlantic croaker of both sexes were captured by shrimp trawl from Redfish Bay, Texas, during the late summer and maintained in the laboratory in large tanks with a recirculating sea water system. Croaker undergo gonadal recrudescence in the laboratory under a simulated seasonal cycle of photoperiod/water temperature and are routinely maintained at the fully recrudesced stage under fall photoperiod (light-dark cycle, 12L:12D) and temperature (22 ± 1°C) conditions until February–March. Experiments with croaker (35–50 g) during early gonadal recrudescence (gonadosomatic index, GSIs = < 0.7) were conducted in September, with the late-recrudescing individuals (65–80 g; GSIs = 8–10) in November, and with fully recrudesced fish (75–90 g; postvitellogenic females: GSIs = 14–17; spermiating males: GSIs = 8–12) during December–January. Approximately 1000 fish were killed for the experiments included in the present study.
Chemicals and Drugs
The LHRHa ([Des-Gly10,D-Arg6,Trp7,Leu8,Pro9]-LHRH, ethylamide) was purchased from Bachem California (Torrance, CA). 1,4,6-Androstatrien-3,17-dione was obtained from Steraloids Inc. (Wilton, NH). Estradiol-17ß, testosterone, 5-dihydrotestosterone, iodogen, and other analytical-grade chemicals were purchased from Sigma Chemical Co. (St. Louis, MO).
Experimental Protocols
Experiments were conducted in 1500-liter recirculating sea water tanks (20–25 fish/tank). All the surgical procedures were performed under deep anesthesia with quinaldine sulphate (20 mg/L). Fish from each tank were divided into two subgroups on the day of termination of the experiments. They received i.p. injections in the morning (0800–1000 h) of either fish saline or LHRHa dissolved in saline. A total of 10–12 fish from each subgroup were bled under anesthesia 3 h after the injections (always between 1100 and 1300 h to avoid diurnal influences; < 10 min sampling time/group). Plasma samples collected after 20-min centrifugation were stored at -20°C until assayed for GTH II levels. Pituitaries were collected and stored at -80°C for the analysis of pituitary GTH II content. The gonad and body weights were recorded to calculate GSIs (gonad weight expressed as percent body weight) in the case of gonad-intact fish. The GSIs for gonadectomized fish were determined at the time of surgery.
Gonadectomy and Sham-Operation
All surgical operations were performed in a clean operating hood fitted with a UV light source that was turned on during the period between each surgery to keep the operating area clean. Fish were anesthetized, and gonads were removed through a 2- to 3-cm incision in the abdomen. The wound was sutured with a silk thread. A similar surgery was performed for sham-operation except that the gonads were not removed. All the fish were given penicillin after the surgery to prevent bacterial infection. Fish resumed their normal eating patterns within 24 h after the surgery, and the wounds were completely healed within one week. Completeness of gonadectomy was confirmed by visual examination at the time of sampling in all the gonadectomized fish, and no sign of gonadal regeneration was detected in any specimen.
Steroid Implants
Pieces of Silastic (Dow Corning Co, Midland, MI) tubing (1 cm long, 1.55-mm internal diameter, 0.8-mm wall thickness) were filled with the desired amount of steroids (10 µg/g BW), and the ends were closed with silicone adhesive. The tubing was presoaked in fish saline overnight before it was inserted in the body cavity through a 4- to 5-mm incision. Empty tubing was implanted in the blank control groups. The steroid capsules were implanted in gonadectomized or sham-operated fish, 14–17 days after the initial surgery.
Experiment 1. Effects of Gonadectomy and Steroid Administration in Spermiating Males
Spermiating males were gonadectomized (Gx) and sham-operated (Sham-Gx), and allowed to recover for 2 wk after the surgery. Sham-Gx and Gx croaker were divided in two groups of 22–24 fish each and received implants of either capsules containing testosterone (+T; 10 µg/g BW) or empty capsules (+Blank), 2 wk after the initial surgery. Each group was further divided into two subgroups (n = 10–12) and injected i.p. with either fish saline or LHRHa (5 ng/g BW), five days after the implants. Blood and pituitary samples were collected 3 h after the injections for measurement of plasma GTH II and steroid levels, and pituitary GTH II content. Similar experimental protocols were used to test the effects of estradiol (+E2) and 5-dihydrotestosterone (+DHT) treatments.
Experiment 2. Effects of Gonadectomy and Steroid Administration in Late-Recrudescing and Fully Recrudesced Females
Late-recrudescing and fully recrudesced females were gonadectomized or sham-operated and then received implants of capsules containing either the steroids (testosterone, estradiol, or 5-dihydrotestosterone; 10 µg/g BW), or empty capsules, 2 wk later. Five days after the implants, fish were divided in two subgroups (n = 10–12), given injections of either saline or LHRHa (5 ng/g BW), and sampled according to the protocols described in experiment 1.
Experiment 3. Effects of an Aromatase Inhibitor and Testosterone in Males and Females
Gonad-intact spermiating males and Gx fish of either sex first received implants of Silastic capsules containing 1,4,6-androstatrien-3,17-dione (+ATD; 10 µg/g BW), an aromatase inhibitor, or empty capsules. Two days after the first set of implants, they were given capsules with testosterone or empty capsules. Fish were divided into two subgroups (n = 10–12) and received injections of either saline or LHRHa (5 ng/g BW) five days after the second set of implants. Blood samples were collected 3 h after the injections.
Experiment 4. Effects of Testosterone and Estradiol in Females During Early Recrudescence
The steroids were first dissolved in ethanol and then mixed with peanut oil according to the protocol described by Pankhurst et al. [34]. Three groups of 20–24 fish each were given three i.p. injections of testosterone or estradiol (0.1 µg/g BW/injection), or vehicle alone, on alternate days. Fish from each group were divided into two subgroups (n = 10–12) and were administered either saline or LHRHa (50 ng/g BW) 24 h after the third injection. Blood and pituitary samples were collected 3 h after the injections for analysis of plasma GTH II and steroid levels, and pituitary GTH II content.
Gonadotropin Assay
GTH II levels were measured in 100 µl plasma or diluted pituitary extract by homologous RIA as described previously [35]. Pituitaries were homogenized in the protein assay buffer (0.05 M PBS, 0.1 M EDTA, 0.05% BSA, pH 7.6) and centrifuged, and the supernatants were diluted in the buffer (5000- to 10 000-fold final dilution) before the GTH II assay. The croaker GTH II antibody has been well characterized and shows low cross-reactivity (15%) with GTH I [36]. The assay has a sensitivity of 5 pg/tube equivalent to 50 pg/ml plasma sample. Interassay variance was 7.8%, and the recovery of GTH II added to croaker plasma ranged between 81% and 108%.
Steroid Assays
Plasma testosterone and estradiol levels were determined by steroid RIA following the general procedures previously described [37] and validated for hormone measurement in croaker plasma.
Statistical Analyses
Data were analyzed by one-way ANOVA. Individual group means were compared using Tukey's HSD test. Differences in plasma steroid concentrations between the late recrudescence and fully recrudesced stages of the gonadal cycle were compared by Student's t-test assuming unequal variances. Differences were considered significant at the p < 0.05 level for all the experiments.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Experiment 1. Effects of Gonadectomy and Steroid Administration in Spermiating Males
Gonadectomy of spermiating males caused a 2- to 3-fold increase in LHRHa-induced GTH II secretion without altering basal hormone secretion (Fig. 1). The increased gonadotropin response to stimulation by LHRHa in Gx fish was completely blocked by treatment with testosterone and estradiol. In addition, both testosterone and estradiol significantly inhibited LHRHa-induced GTH II secretion in gonad-intact (Sham-Gx) spermiating males (Fig. 1, A and B). Estradiol, but not testosterone, also stimulated basal GTH II secretion in Gx males compared to the fish implanted with blank capsules (Fig. 1B). The nonaromatizable androgen, 5-dihydrotestosterone, failed to alter basal or LHRHa-induced GTH II secretion (Fig. 1C). There were no significant changes in pituitary GTH II content after gonadectomy or testosterone replacement (data not included). Plasma testosterone levels at the time of the termination of the experiment presented in Figure 1A were 2.23 ± 0.36 in Sham-Gx+Blank, 7.22 ± 0.83 in Sham-Gx+T, 0.27 ± 0.05 in Gx+Blank, and 5.94 ± 0.75 ng/ml in Gx+T groups. Plasma estradiol levels in the experiment presented in Figure 1B were 0.21 ± 0.05 in Sham-Gx+Blank, 3.96 ± 0.62 in Sham-Gx+E2, nondetectable in Gx+Blank, and 3.81 ± 0.57 ng/ml in Gx+E2 groups.
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Experiment 2. Effects of Gonadectomy and Steroid Administration in Late-Recrudescing and Fully Recrudesced Females
Gonadectomy of the late-recrudescing and fully recrudesced females induced an increase in the gonadotropin response to LHRHa (Fig. 2). However, gonadectomy of females at both these stages of the ovarian cycle did not alter basal GTH II secretion. The enhanced gonadotropin response to LHRHa in Gx fish was significantly decreased by testosterone, but not by estradiol treatment, in the late-recrudescing individuals (Fig. 2A). In contrast, estradiol treatment significantly decreased the response to LHRHa when gonadectomy was performed on fully recrudesced females (Fig. 2B). Treatment of Gx fish at this stage with 5-dihydrotestosterone also caused an apparent decline (40%) in LHRHa-induced GTH II secretion, but the decrease was not significant (p < 0.076). In addition, estradiol stimulated basal GTH II secretion in gonad-intact and Gx females during the late-recrudescence phase of the gonadal cycle. A stimulatory effect of estradiol implants on basal GTH II secretion was also observed in fully recrudesced fish after gonadectomy. Pituitary GTH II content was not significantly altered by any of these treatments (data not included). Mean plasma testosterone and estradiol levels at the time of termination of the experiment in croaker implanted with the respective steroids were 5.48 ± 0.35 and 4.63 ± 0.54 ng/ml in Sham-Gx, and 4.68 ± 0.77 and 3.58 ± 0.42 ng/ml in Gx fish. Both testosterone and estradiol levels in gonad-intact females declined significantly in croaker with fully developed gonads compared to those in late-recrudescing fish (testosterone: 1.43 ± 0.11 versus 2.50 ± 0.35 ng/ml; estradiol: 0.87 ± 0.08 versus 1.54 ± 0.13 ng/ml).
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Experiment 3. Effects of an Aromatase Inhibitor and Testosterone in Males and Females
Preimplantation of 1,4,6-androstatrien-3,17-dione (10 µg/g BW), an aromatase inhibitor, completely blocked the negative influence of testosterone on LHRHa-induced GTH II secretion in both gonad-intact (Fig. 3A) and Gx (Fig. 3B) spermiating males. However, the aromatase inhibitor only partially blocked the inhibitory effect of testosterone on LHRHa-induced GTH II secretion in females that were gonadectomized at the fully recrudesced stage (Fig. 3C). This experiment with females was repeated to confirm the results. Mean plasma testosterone levels in spermiating males at the time of termination of the experiments were 1.35 ± 0.09 in gonad-intact, 5.43 ± 0.48 in testosterone-implanted, nondetectable in Gx+Blank, and 4.43 ± 0.59 ng/ml in Gx+T groups. In females, mean testosterone levels in the two groups given testosterone implants (n = 22) were 6.15 ± 0.68 ng/ml. Plasma steroid levels were not significantly different between T-implanted and ATD+T-implanted groups.
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Experiment 4. Effects of Testosterone and Estradiol in Females During Early Recrudescence
Testosterone and estradiol treatments significantly stimulated both basal and LHRHa-induced GTH II secretion in croaker during the early-recrudescence phase of the gonadal cycle (Fig. 4A). In addition, testosterone elicited a significant increase in pituitary GTH II content (Fig. 4B). There was also a trend of elevated pituitary GTH II concentrations after estradiol treatment, but the increase was not significant. Plasma testosterone and estradiol levels, respectively, at the time of the termination of the experiment were 2.84 ± 0.36 and 1.74 ± 0.33 ng/ml in vehicle-treated, 5.12 ± 0.69 and 2.48 ± 0.44 ng/ml in testosterone-treated, and 3.08 ± 0.66 and 4.16 ± 0.55 ng/ml in estradiol-treated groups.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Positive effects of gonadal steroids on both basal and LHRHa-induced GTH II secretion in adults have not been demonstrated previously in the same teleost species. However, there is evidence that the gonads exert a positive influence on basal GTH II secretion in adult male Atlantic salmon throughout gonadal recrudescence [18]. In addition, the potentiating effect of testosterone and estradiol on LHRHa-induced GTH II secretion observed during the early-recrudescence phase of the gonadal cycle in croaker is comparable to that reported for goldfish [19]. The stimulatory effect of steroids on basal GTH II secretion in immature rainbow trout and European eel has been suggested to involve enhanced GnRH synthesis and release [13, 38]. However, it is not known whether a similar mechanism operates in adult teleosts. On the other hand, it has been shown in early-recrudescing rainbow trout and goldfish that steroids can act directly at the pituitary to potentiate the effect of LHRHa on in vitro GTH II release [20, 39]. Therefore, the stimulation of basal and LHRHa-induced GTH II secretion by gonadal steroids could potentially involve two different mechanisms. Moreover, the increases in plasma and pituitary GTH II concentrations during the early-recrudescence phase in croaker indicate that both the synthesis and release of the hormone are augmented by the steroid treatments.
The gonadectomy-induced increase in gonadotropin response to LHRHa during the later stages of gonadal recrudescence in both male and female croaker is similar to that previously observed in castrated African catfish [12]. Although testosterone and estradiol treatments reversed the effect of gonadectomy on LHRHa-induced GTH II secretion in both male and female croaker with fully developed gonads, estradiol was only partially effective in females gonadectomized during the late-recrudescence phase of the gonadal cycle. These results suggest that the negative effect of testosterone appears first during ovarian recrudescence in croaker and that of estradiol begins later when the ovaries have fully recrudesced. Negative effects of testosterone and estradiol on LHRHa-induced GTH II secretion similar to those observed in croaker have not been reported previously in teleosts, although suppression of LHRHa-induced GTH II secretion has been observed in castrated African catfish treated with androstenedione [12]. In addition, comparable negative effects of gonadal steroids on LHRH-induced LH secretion have been demonstrated previously in tetrapods [2–6]. Administration of testosterone or estradiol also inhibits LHRHa-induced GTH II secretion in spermiating male croaker with intact gonads, whereas in females endogenous gonadal input has to be removed to demonstrate the negative feedback.
No evidence was obtained for a gonadal and steroid negative feedback on basal GTH II secretion when presumably the gonadotrophs are stimulated with low levels of endogenous GnRH. A similar lack of gonadal negative feedback on basal GTH II secretion has recently been reported in male Atlantic salmon [18]. In other salmonids, catfish, and goldfish, gonadectomy increases and steroid treatment suppresses basal GTH II secretion [7, 8, 10]. The reason for these differences is not known, but may be related to possible species differences in the set points of endogenous GnRH release in the pituitary at which steroids begin to exert their negative effects on GTH II secretion. Negative feedback of gonadal steroids is exerted on both basal and LHRHa-induced LH secretion in most tetrapods [3–6]. Therefore, Atlantic croaker provides an interesting vertebrate model for investigating the mechanisms of negative feedback on LHRHa-induced GTH II secretion without the complication of alterations in basal GTH II secretion. Other gonadal factors such as activin and inhibin have been shown to stimulate GTH II release in goldfish [40]. However, the lack of a significant effect of gonadectomy on basal GTH II secretion and complete reversal of the effect of gonadectomy on LHRHa-induced GTH II secretion by steroid replacement suggest that these factors do not exert a profound influence on GTH II secretion in croaker with fully developed gonads.
The experiments with an aromatase inhibitor suggest that the negative effect of testosterone on LHRHa-induced GTH II secretion demonstrated in fully recrudesced croaker is mediated by its conversion to estradiol in the brain and/or pituitary gland. Similarly, previous studies indicate that the negative effect of testosterone on basal gonadotropin secretion in African catfish and the positive effect on LHRHa-induced GTH II secretion in goldfish involves aromatization of testosterone to estradiol [8, 19]. Moreover, evidence has been obtained that aromatase activity in the brains of mature Atlantic salmon is up-regulated by testosterone [25]. Therefore, testosterone could potentially increase estrogen availability by increasing aromatase activity as well as providing substrate for the enzyme.
The observation that an aromatase inhibitor completely reversed the inhibitory influence of testosterone on LHRHa-induced GTH II secretion in males, but only partially blocked it in females, suggests that there are sex differences in the negative feedback control of GTH II secretion in croaker. This possibility is further supported by the finding that 5-dihydrotestosterone partially blocked LHRHa-induced GTH II secretion in Gx females but was ineffective in males. Taken together, these results suggest that part of the negative effect of testosterone on LHRHa-induced GTH II secretion in female croaker may be by a direct action mediated via an androgen receptor. 5-Dihydrotestosterone could potentially exert its influence on GTH II secretion by binding to one of the two androgen receptors (ARs) recently characterized in croaker that has a high binding affinity for the steroid [41]. The discovery of two ARs in croaker [41] and rainbow trout (GenBank Accession #AB012095 for AR and AB012096 for ARß) raises the question of which of the two ARs mediates the negative control by testosterone in females.
The mechanisms by which gonadal steroids stimulate basal GTH II secretion and inhibit LHRHa-induced secretion in Gx fish of both sexes under the same experimental conditions, and their sites of action, are unclear at present. The effects could be exerted on the GnRH cell bodies in the preoptic-anterior hypothalamic area, nerve terminals in the teleostean pituitary, or directly on the gonadotrophs by altering GnRH receptor concentrations. The demonstration that gonadal steroids only exert a negative effect on LHRHa-induced GTH II secretion in croaker suggests that the steroids might act directly at the pituitary level. GnRH receptor concentrations in the pituitary are increased by gonadectomy in rats and African catfish and are decreased by estradiol in rats and by androstenedione in the catfish [12, 42]. Although GnRH receptor concentrations were not measured in croaker, a mechanism similar to that in the catfish and rat could be responsible for the negative feedback in this species.
Steroid receptors are not present on GnRH neurons in mammals and fishes but are located on adjacent neurons containing various neurotransmitters, such as monoamines and GABA [43–46]. These neurotransmitters have been shown to mediate some of the effects of gonadal steroids in both mammals and fishes [1, 26–28]. Serotonin (5-HT) potentiates LHRHa-induced GTH II secretion primarily via 5-HT2 receptors in fully recrudesced croaker but not in gonadally regressed individuals [30, 31]. Thus, it is possible that gonadal steroids may modulate serotonergic influences on GTH II secretion in croaker. Dopamine (DA) has been implicated in mediating steroid effects on GTH II secretion in several teleosts [1]. However, DA is unlikely to be involved in steroid feedback regulation of GTH II secretion in croaker because DA does not exert an inhibitory control on GTH II secretion in croaker or other perciform fishes [17, 32]. On the other hand, GABA stimulates basal GTH II secretion in gonadally regressed croaker and inhibits it in fully recrudesced fish [30]. Moreover, GABA does not alter LHRHa-induced GTH II secretion at any stage of the gonadal cycle in croaker, a situation similar to that in goldfish [1, 29]. Therefore, GABA is unlikely to mediate the negative effect on LHRHa-induced GTH II secretion, but it may be involved in mediating the positive effect on basal hormone secretion in croaker.
In conclusion, testosterone and estradiol stimulate basal and LHRHa-induced GTH II secretion in croaker during early gonadal recrudescence, and the influence decreases during the late-recrudescence phase when only a slight stimulatory influence of estradiol on basal GTH II secretion is detected. The influence of the gonadal steroids switches to a negative one on LHRHa-induced GTH II secretion once the fish have fully developed gonads. Plasma levels of the two steroids decline at the end of ovarian recrudescence, which probably diminishes their inhibitory influence on GnRH-induced GTH II secretion. The removal of negative feedback presumably enables the ovulatory GTH II surge to occur in response to the neurochemical signals triggered by the appropriate environmental and social cues for spawning. Despite differences in the details of feedback influences, the existence of a negative effect of gonadal steroids on GnRH-induced GTH II secretion in a teleost, Atlantic croaker, similar to that in tetrapods suggests that this mechanism is highly conserved in vertebrates.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Correspondence: Izhar A. Khan, The University of Texas at Austin, Marine Science Institute, 750 Channelview Drive, Port Aransas, TX 78373. FAX: 512 749 6777; ikhan{at}utmsi.utexas.edu
Accepted: April 29, 1999.
Received: January 20, 1999.
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