Serum GtH Levels Research Articles

A reduction in pituitary dopamine turnover is associated with sex pheromone-induced gonadotropin secretion in male goldfish

In goldfish, the gonadal steroid, 17α,20β-dihydroxy-4-pregnen-3-one (17,20β-P), functions as a potent preovulatory female sex pheromone which stimulates rapid elevations in serum gonadotropin (GtH) levels and subsequent increases in milt production in males. GtH secretion in goldfish is known to be regulated by the stimulatory actions of gonadotropin-releasing hormone (GnRH) and the inhibitory actions of dopamine (DA). This study specifically examined whether the 17,20β-P-induced elevation in male GtH is caused by pheromone-mediated changes in DA inhibition at the level of the pituitary. First, we have demonstrated that dihydroxyphenylacetic acid (DOPAC) is the primary metabolite of DA catabolism in the brain and pituitary gland of goldfish. Second, we measured changes in circulating levels of GtH and changes in pituitary content of DA and its metabolite, DOPAC, as well as possible alterations in DA turnover rate (DOPAC/DA ratio) following short-term exposure of male goldfish to water-borne 17,20β-P. Water-borne 17,20β-P consistently increased serum GtH levels in males within 20 min of exposure and maintained elevated levels for up to 120 min. Although changes in pituitary DA content were not observed during periods of high GtH release, coincident reductions in pituitary levels of DOPAC were measured within 45 min of exposure to the pheromone. More importantly, there was a significant decrease in the rate of DA turnover in the pituitary, as assessed by comparing the ratio of DOPAC to DA present, at 20, 45, and 120 min of exposure. Since the reduction of DA turnover in the pituitary is inversely correlated with periods of increased GtH release, the present results suggest that water-borne 17,20β-P causes an abatement of DA release to the pituitary. Based on the latency of the GtH response to water-borne 17,20β-P, a rapid reduction of DA turnover in the pituitary appears to be at least part of the neuroendocrine trigger for 17,20β-P-induced GtH release in male goldfish.

Stimulation of pituitary gonadotropin and ovarian development by chronic administration of testosterone in female Japanese silver eel, Anguilla japonica

Serial implantation of testosterone pellets, at 30-day intervals to day 75 or at 15-day intervals to day 105, stimulated the pituitary content of gonadotropin (GtH) to increase approximately 24 fold; however, no significant changes in serum GtH levels were detected at the sampling times used. Vitellogenesis was stimulated in the ovary of all testosterone-implanted animals; the ovary of at least one eel appeared to be at a preovulatory state (gonadosomatic index = 39.8%), as demonstrated by the presence of large yolky oocytes. Serial implantation of LHRH-A or domperidone along with testosterone did not further stimulate pituitary GtH content or ovarian development. The results demonstrate that chronic treatment with testosterone alone can stimulate the brain-pituitary-ovary axis of the Japanese silver eel to induce ovarian development to, or nearly to, the prespawning stage.

Testosterone and Estradiol Potentiate the Serum Gonadotropin Response to Gonadotropin-Releasing Hormone in Goldfish1

The effects of gonadal steroids on gonadosomatic index (GSI; gonad wt/total body wt x 100), pituitary gonadotropin (GTH) content, and serum GTH response to [D-Ala6,Pro9-Net]-luteinizing hormone-releasing hormone (LHRH-A) were investigated throughout the seasonal reproductive cycle of the goldfish. Gonad-intact female fish were implanted i.p. for 5 days with silastic pellets containing no steroid (blank), testosterone (T; 100 micrograms/g), or estradiol (E2; 100 micrograms/g). The serum GTH response at 6 h following i.p. injection of saline or 0.1 microgram/g LHRH-A was assessed. In blank-implanted, saline-injected animals, seasonal variations in GSI, pituitary GTH content, and serum GTH levels were evident; maximal and minimal levels were noted in the spring and summer months, respectively. In blank-implanted fish, LHRH-A effectively stimulated GTH release in females undergoing gonadal recrudescence (late autumn and winter) and in sexually mature (spring) females, but not in sexually regressed (summer and early autumn) females. Implantation of T or E2 raised serum steroid levels to those found during ovulation in goldfish. Steroid treatments did not affect unstimulated serum GTH levels at any time of the year. Testosterone effectively potentiated the serum GTH response to LHRH-A during the entire reproductive cycle, whereas the positive effects of E2 were evident in sexually regressed and post-spawning females only. Both T and E2 potentiated the GTH response to LHRH-A in male fish. To examine the involvement of T aromatization in mediating its actions on induced GTH secretion, male and female fish were implanted with T or the nonaromatizable androgens 5 alpha-dihydroxytestosterone (DHT; 100 micrograms/g) and 11-keto-testosterone (11-KT; 250 micrograms/animal). Testosterone potentiated the GTH response to LHRH-A in both males and females whereas DHT and 11-KT were without effect. Furthermore, the positive action of T on induced GTH secretion was blocked by 2-day pretreatment with the aromatase inhibitor 1,4,6-androstatrien-3,17-dione (100 or 300 micrograms/g). Multiple i.p. injections of hCG (0.2 microgram/g every 3 days for 39 days), probably through stimulation of endogenous T secretion, resulted in potentiation of the GTH response to LHRH-A in mature male goldfish. These results clearly demonstrate that T, through aromatization to E2, can increase pituitary responsiveness to exogenous LHRH-A in gonad-intact male and female goldfish.

Effects of gonadotropin-releasing hormone agonists and dopamine antagonists on gonadotropin secretion and ovulation in Chinese loach, Paramisgurnus dabryanus

The analogs [D-Ala 6, Pro 9NEt]-luteinizing hormone-releasing hormone (LHRH-A) and [D-Arg 6, Pro 9NEt]-salmon gonadotropin-releasing hormone (sGnRH-A) were tested in the presence or absence of pimozide (PIM) or domperidone (DOM) for their ability to stimulate an increase in serum gonadotropin (GtH) levels and ovulation in preovulatory female loach. In the absence or presence of PIM or DOM, sGnRH-A was more active than LHRH-A in terms of stimulating serum GtH levels. PIM or DOM potentiated the activity of both peptides equally. PIM or DOM (5 μg/g body weight) plus 0.001 μg/g body weight of sGnRH-A were effective in stimulating serum GtH levels and a good rate of ovulation (50–70%). The most effective combination for inducing ovulation (100%) was sGnRH-A at 0001 μg/g body weight plus DOM at 5 μg/g body weight. LHRH-A at 0.001 μg/g body weight and PIM or DOM (5 μg/g body weight) were ineffective in inducing a good rate of ovulation. These results indicate that GnRH-A in the presence of DOM or PIM is effective in stimulating ovulation in loach at dosages about 10-fold less than for LHRH-A. The time to ovulation following injection of DOM plus sGnRH-A was highly predictable, in the range of 11–14 h postinjection.

Changes in brain levels of gonadotropin-releasing hormone and serum levels of gonadotropin and growth hormone in goldfish during spawning

Changes in serum levels of gonadotropin (GtH) and growth hormone (GH) and in levels of gonadotropin-releasing hormone (GnRH) in the pituitary and discrete brain areas were studied in male goldfish during spawning with spontaneously ovulating females. Spontaneous ovulation in females was induced by raising water temperature from 12 to 20 °C and providing spawning substrate of artificial floating vegetation. Spawning occurs naturally in sexually mature male goldfish in the presence of ovulating females. Serum GtH levels in spawning male goldfish exposed to ovulatory females increased markedly in synchrony with the ovulatory GtH surge in females. There was also a significant increase in serum GH levels in the spawning males. GnRH levels in the olfactory bulbs, telencephalon, hypothalamus, and pituitary of the spawning males showed marked decreases at the same time as serum levels of both GtH and GH peaked; these events in the males corresponded to the approximate time of ovulation, and similar changes in serum GtH and GH levels and brain GnRH levels, in the females. This temporal correlation between changes in GnRH levels in the brain and pituitary and increases in serum levels of GtH and GH in males as well as females supports the idea that activation of the GnRH neuronal system may be a common pathway for the stimulation of pituitary GtH and GH secretion in goldfish during spawning.

Alterations in gonadotropin-releasing hormone immunoactivities in discrete brain areas of male goldfish during spawning behavior

In male goldfish, spawning behavior and gonadotropin (GtH) secretion are stimulated during exposure to females which were induced to perform spawning behavior by treatment with prostaglandin F2α (PG). In this study, exposure to PG-treated females for 1 or 2 h significantly increased serum GtH levels, and GtH-releasing hormone (GnRH) concentrations in the olfactory bulbs, telencephalon and hypothalamus, indicating that spawning behavior can influence cellular events of the brain GnRH neuronal system and pituitary GtH secretion in male goldfish. To study the role of the olfactory system in the hormonal responses to PG-treated females, bilateral sectioning of olfactory tracts (OTX), medial (mOTX) or lateral (1OTX) olfactory tract were carried out in male goldfish. Both OTX and mOTX, but not 1OTX, blocked the behavioral response of male goldfish to PG-treated females and abolished the increases in serum GtH and brain GnRH levels, suggesting that alterations in pituitary GtH secretion and brain GnRH levels are associated with a pheromonal activation of spawning behavior through the medial olfactory tracts in male goldfish. This behavioral activation of the GnRH neuronal system provides a useful physiological model for studying the regulation of GnRH system in male goldfish.

Seasonal changes in serum gonadotropin, testosterone, 11-ketotestosterone, and estradiol-17β levels and their relation to tumor burden in gonadal tumor-bearing carp × goldfish hybrids in the Great Lakes

The hybrids of carp ( Cyprinus carpio) and goldfish ( Carassius auratus) collected from the lower Great Lakes between 1978 and 1981 exhibited a high frequency of gonadal neoplasms and apparent sterility, conditions which were rare in the parental species. A pronounced hyperplasia of fonadotropic cells in hybrids resulted in the accumulation of large stores of biologically active gonadotropin (GtH) in the pituitary gland. Serum GtH levels were generally higher in hybrids than in carp collected from the same areas, but seasonal trends were similar for both species. Among hybrids, tumored individuals had higher serum GtH levels than nontumored individuals. Serum levels and seasonal trends for testosterone (T), 11-ketotestosterone (11-KT), and estradiol-17β (E2) were, for the most part, similar when carp and nontumored hybrids of the same gender were compared. Serum levels of T and 11-KT (but not E2) were generally higher in tumored hybrids when compared to nontumored individuals. High serum steroid levels were related to a specific tumor type, possibly of Sertoli cell origin. Although the etiology of the gonadal tumors is not yet known, the serum levels of gonadal steroids in hybrids make it unlikely that a lack of steroidal feedback is responsible for the gonadotrop hyperplasia.

Pituitary gonadotropin-releasing hormone (GnRH) receptor activity in goldfish and catfish: seasonal and gonadal effects

The goldfish pituitary contains two classes of gonadotropin-releasing hormone (GnRH) binding sites, a high affinity/low capacity site and a low affinity/high capacity site (Habibiet al. 1987a), whereas the catfish pituitary contains a single class of high affinity GnRH binding sites (De Leeuwet al. 1988a). Seasonal variations in pituitary GnRH receptor binding parameters, and the effect of castration on pituitary GnRH receptor binding were investigated in goldfish and catfish, respectively. In goldfish, GnRH receptors undergo seasonal variation with the highest pituitary content of both high and low affinity sites occurring during the late stages of gonadal recrudescence. The observed changes in pituitary GnRH receptor content correlate closely with responsiveness to a GnRH agonistin vivo in terms of serum gonadotropin (GTH) levels. In catfish, castration results in a two-fold increase in pituitary GnRH receptor content, which can be reversed by concomitant treatment with androstenedione, but not by the non-aromatizable androgen 11β-hydroxyandrostenedione; changes observed in GnRH receptor content correlate with variations in serum GTH levels and responsiveness to a GnRH agonist. In summary, the present study provides a clear evidence for seasonal variation in pituitary GnRH receptor activity in goldfish, and demonstrates a gonadal feedback mechanism regulating GnRH receptor activity in the catfish pituitary.

Hypothalamic peptides influencing growth hormone secretion in the goldfish,Carassius auratus

In vivo andin vitro techniques were used to examine the influence of various vertebrate peptides on growth hormone (GH) secretion in the goldfish. Tetradecapeptide somatostatin (SRIF-14) was found to inhibit GH secretionin vitro from perifused pituitary fragments, whereas similar concentrations of a salmonid SRIF peptide (sSRIF-25) did not affect GH secretion from the goldfish pituitary fragments. This indicates that SRIF receptors on the goldfish pituitary are very specific for SRIF-14-like peptides. Salmon gonadotropin (GTH)-releasing hormone (sGnRH) was found to elevate serum GH levels in male goldfish. The dopamine antagonist pimozide alone or injected in combination with sGnRH did not influence serum GH levels, although injection of pimozide alone significantly elevated serum GTH levels, in addition to potentiating the effects of sGnRH on GTH secretion. sGnRH stimulated GH secretion from goldfish pituitary fragmentsin vitro, indicating that sGnRH acts directly at the level of the pituitary to stimulate GH secretion in the goldfish. These results suggest that GnRH may also function as a GH-releasing factor in the goldfish, although the release-inhibitory factors for GH and GTH secretion do appear to be separate and distinct. Two human GH-releasing hormone (hGHRH) peptides were found to be ineffective in altering GH secretionin vitro from the perifused pituitary fragments. Consequently, a role for a mammalian GHRH-like peptide in the hypothalamic regulation of GH secretion in the goldfish remains questionable.

Serotonin stimulates gonadotropin release in female and male goldfish, Carassius auratus L

Effects of serotonin (5-HT) on serum gonadotropin (GtH) levels were studied in female and male goldfish, Carassius auratus L. Intraperintoneal (ip) administration of 5-HT (10 μ/g) produced a significant increase in serum levels of GtH at 0.5, 1, and 2 hr but not at 3–4 hours, after the drug was injected. Adminstration of different concentrations of 5-HT into the brain third ventricle (iv) did not affect serum GtH levels. In both sexes, the intraperitoneal administration of different doses of 5-HT (2.5–20 μg/g) caused a dose-dependent increase in serum GtH levels in fish at different gonadal stages; the greatest responses occurred in mature (=prespawning) fish. Fluoxetine (10 μg/g; ip), a 5-HT reuptake inhibitor, potentiated the stimulatory effects of 5-HT on GtH secretion. Ketanserin (10 μg/g; ip), a 5-HT antagonist, did not modify basal GtH levels; however, ketanserin blocked the 5-HT induced release of GtH. These results indicate that 5-HT has a stimulatory effect on GtH release in goldfish, most likely at the level of the pituitary gland.

Comparison of [D-Arg6, Trp7, Leu8, Pro9NEt]-luteinizing hormone-releasing hormone (sGnRH-A), and [D-Ala6, Pro9NEt]-luteinizing hormone-releasing hormone (LHRH-A), in combination with pimozide, in stimulating gonadotropin release and ovulation in the goldfish, Carassius auratus

LHRH-A and sGnRH-A were tested, in the presence or absence of pimozide (Pim), for their ability to stimulate increases in serum gonadotropin (GtH) levels and ovulation in prespawning female goldfish. In the absence of Pim, sGnRH-A was more active than LHRH-A in terms of stimulating serum GtH levels; neither peptide given alone was effective in stimulating ovulation. Pim potentiated the activity of both peptides; high dosages of either peptide, plus a high dosage of Pim, were highly effective in stimulating serum GtH and ovulation. A low dosage of sGnRH-A, plus a low dosage of Pim, were also effective in stimulating serum GtH and ovulation; however, a low dosage of LHRH-A plus a low dosage of Pim were ineffective. The time to ovulation following injections, for those treatments that were highly effective in inducing ovulation, was highly predictable, and oocyte fertility and viability were high. These results indicate that sGnRH-A, in the presence of Pim, is effective in stimulating ovulation in goldfish at dosages about 10-fold less than for LHRH-A. The basis for the differences in potency between sGnRH-A and LHRH-A is discussed.

Effects of [ d-Ala 6, Pro 9-NEt]-LHRH and catecholaminergic drugs on gonadotropin secretion and ovulation in the Chinese loach ( Paramisgurnus dabryanus)

The effects of [ d-Ala 6, Pro 9-NEt]-LHRH (LHRH-A) alone and in combination with drugs which influence the actions of dopamine or the synthesis of catecholamines on gonadotropin (GtH) secretion and ovulation in the loach ( Paramisgurnus dabryanus) were investigated. LHRH-A alone stimulated an increase in serum GtH levels in the loach, but was a relatively ineffective treatment for the induction of ovulation. Injection of the dopamine receptor antagonist pimozide caused a marked potentiation of the GtH-release response to LHRH-A, and combined injections of pimozide and LHRH-A were an effective treatment for the induction of ovulation. Reserpine, a drug which causes depletion of catecholamines from presynaptic terminals, also caused a marked potentiation of the GtH-release response to LHRH-A and combined treatment induced ovulation. Similarly, administration of α-methyl- para-tyrosine to block conversion of tyrosine to l-dopa, or carbidopa to block conversion of l-dopa to dopamine, potentiated the GtH-release response to LHRH-A and induced ovulation. In contrast, the use of diethyldithiocarbamate, to block conversion of dopamine to norepinephrine, failed to augment the action of LHRH-A on GtH release and ovulation. The present results provide further evidence to suggest that dopamine functions as a gonadotropin release-inhibitory factor in teleosts, and demonstrate that the use of drugs which block either the synthesis or the actions of dopamine potentiates the action of LHRH-A in teleosts.

The effects of different doses of pimozide and [D-Ala6, Pro9-N ethylamide]-LHRH (LHRH-A) on gonadotropin release and ovulation in female goldfish

Female goldfish, in late stages of ovarian recrudescence, held at 12 or 20 °C, were injected with a range of dosages of the dopamine antagonist pimozide, at 10, 1, and 0.1 μg/g body weight, to block the endogenous gonadotropin release inhibitory activity of dopamine, and 3 h later were injected with [D-Ala6, Pro9-N ethylamide]-luteinizing hormone-releasing hormone (LHRH-A), at 0.1 μg/g body weight, after which serum gonadotropin levels were determined. The results demonstrate the dose dependency of pimozide in potentiating the activity of LHRH-A. In a second set of experiments, using female goldfish in a preovulatory condition, held at 12 and 20 °C, the changes in serum gonadotropin levels and frequency of ovulation were determined following injection of pimozide, at 1 μg/g body weight, and LHRH-A, at 0.1, 0.01, and 0.001 μg/g body weight. The results demonstrate that pimozide potentiates a dose-dependent response to LHRH-A. The maximum serum GtH levels found in response to the same dosages of pimozide and LHRH-A at 12 and 20 °C were similar; however, the maximum levels occurred earlier at 20 °C (6 h postinjections) than at 12 °C (24 h postinjections). Notably, only the combination of pimozide at 1 μg/g body weight and LHRH-A at 0.1 μg/g body weight, in fish at 20 °C, was highly effective in inducing ovulation.

Gonadotropin release from the pars distalis of goldfish, Carassius auratus, transplanted beside the brain or into the brain ventricles: Additional evidence for gonadotropin-release-inhibitory factor

The pars distalis of the pituitary was transplanted from one goldfish to another, of matched gonadal condition and body size, either beside the brain (“juxta” location) or into the brain ventricle in the preoptic region or under the optic tectum. Recipients of a pars distalis had significantly higher serum gonadotropin (GtH) levels than sham-operated controls without transplants; following removal of the transplants, serum GtH levels decreased to levels found in controls within 24 hr. This demonstrates that the pars distalis releases GtH spontaneously when removed from its normal connections with the hypothalamus providing evidence for tonic inhibition of GtH release by a GtH-release-inhibitory factor (GRIF). The juxta-transplanted pars distalis of sexually recrudescing and mature ( = completed recrudescence) females released more GtH than the pars distalis of sexually regressed females. The juxta-transplanted pars distalis of sexually mature males released more GtH than the pars distalis of males in early stages of testicular recrudescence. These results demonstrate a seasonal variation in the ability to release GtH independent of GRIF. This may be due to the greater content of GtH in the pituitary, and a greater ability to synthesize GtH by the pituitary in sexually mature and recrudescing goldfish compared to sexually regressed fish. In sexually recrudescing and mature males and females, transplantation of the pars distalis into the brain ventricle in either the preoptic region or ventral to the optic tectum resulted in significantly lower serum GtH levels in recipients than transplantation beside the brain. This demonstrates the presence of some factor in the brain that inhibits GtH release, supporting the idea of GRIF. In sexually regressed female goldfish, GtH release from the transplanted pars distalis was not influenced by location in the brain ventricles versus beside the brain. This suggests a seasonal variation in GRIF activity in the brain, with reduced activity in sexually regressed females coincident with less ability to release GtH by the pars distalis.

Effects of dopamine and apomorphine on gonadotropin release from the transplanted pars distalis in goldfish

Male goldfish bearing pars distalis transplants from other male goldfish have increased serum gonadotropin (GtH) levels, due to the high spontaneous release rate of GtH by the transplants. Intraperitoneal injection of dopamine or its agonist, apomorphine, each reduced the elevated serum GtH levels caused by the release from the transplanted pars distalis. These results suggest that dopamine has GtH-release-inhibitory activity and acts directly on gonadotrophs to inhibit spontaneous secretion of GtH.

Influences of norepinephrine and α-adrenergic mechanisms on gonadotropin secretion in female goldfish, Carassius auratus

Intraperitoneal or intraventricular (3rd cranial ventricle) injection of norepinephrine (NE) caused an increase in serum gonadotropin (GtH) concentrations in female goldfish at times of the year when the ovaries were regressed or at early stages of recrudescence, but had no influence at other stages of the ovarian cycle. In a previous report it was shown that clonidine (α-agonist) increased serum GtH levels in fish at early or mid-ovarian recrudescence [ J. P. Chang, A. F. Cook, and R. E. Peter (1983) Gen. Comp. Endocrinol. 49, 22–31]; however, intraperitoneal injection of clonidine had no effect on circulating GtH levels when tested in fish at late ovarian recrudescence. In fish at early stages of ovarian recrudescence, intraperitoneal injection of phentolamine (α-blocker) did not alter GtH levels, but it blocked the NE-induced increase in serum GtH levels when injected simultaneously with NE. These results suggest that NE stimulates GtH release by α-adrenergic mechanisms at the brain and/or pituitary level in female goldfish in a sexually regressed or early ovarian recrudescence condition.

Induction of ovulation in goldfish, Carassius auratus, by pimozide and analogues of LH-RH

The effects of intraperitoneal injections or pellet implantations of luteinizing hormone-releasing hormone analogues, des-Gly 10-[D-ALA 6]-LH-RH-ethylamide (LRH-Aa) or des-Gly 10-[D-Trp 6]-LH-RH-ethylamide (LRH-At), respectively, and the combination of these treatments with pimozide, a dopamine antagonist, on serum gonadotropin (GtH) and ovulation in goldfish held at 18–20°C were investigated. Injections of LRH-Aa (0.1 μg/g body weight) or pellet implants of LRH-At (25 and 125 μg/fish) alone increased serum GtH levels, but were relatively ineffective for inducing ovulation in goldfish (≅ 25% rate of occurrence). Pimozide greatly potentiated the GtH release response to LRH-Aa injections or LRH-At pellet implantations. A high rate of occurrence of ovulation (87%) was observed within 24 h when pimozide was injected prior to or with the first of two injections of LRH-Aa, or following implantations of LRH-At pellets that give continuous release of LRH-At. These results are consistent with the idea that dopamine acts directly at the pituitary level as a GtH release-inhibitory factor in goldfish.

Effects of pimozide and des Gly 10,[ d-Ala 6]luteinizing hormone-releasing hormone ethylamide on serum gonadotropin concentrations, germinal vesicle migration, and ovulation in female goldfish, Carassius auratus

In gravid female goldfish held at 10–12°, a single injection of des Gly 10,[ d-Ala 6]luteinizing hormone-releasing hormone ethylamide (LHRH-A), or 2 injections of LHRH-A given 12 hr apart, increased serum gonadotropin (GtH) concentrations, but did not stimulate germinal vesicle migration or ovulation. Injection of a dopamine antagonist, pimozide (PIM), increased serum GtH levels. PIM injected with the second of two LHRH-A injections not only potentiated the LHRH-A-induced increase in serum GtH concentrations but also caused germinal vesicle migration and ovulation. PIM injected with, or in place of, the first of two LHRH-A injections increased the frequency of ovulation in fish injected with LHRH-A. Similarly, PIM injected simultaneously with a single LHRH-A injection also increased the number of ovulating fish. These results are consistent with the idea that dopamine inhibits GtH release in goldfish. The results also suggest that the preovulatory surge of GtH secretion is regulated by both a stimulation by GtH-releasing hormone and release from the dopamine inhibition on GtH secretion.

Influence of catecholamines on gonadotropin secretion in goldfish, Carassius auratus

Serum gonadotropin (GtH) concentrations in female goldfish were measured before and at various times after intraperitoneal injection of drugs altering catecholamine synthesis and neural activities. Reserpine, a depleter of neurotransmitter stores, elevated serum GtH levels compared to controls, suggesting the general involvement of neurotransmitters in altering GtH release. 6-Hydroxydopamine, a catecholaminergic neurotoxin, increased serum GtH concentration, suggesting that catecholaminergic neurons inhibit GtH release. Blocking of l-DOPA and dopamine synthesis by α-methyl- para-tyrosine and carbidopa, respectively, but not norepinephrine by diethyldithiocarbamate, raised serum GtH values above those of controls. Injections of an α-agonist, clonidine, also increased serum GtH concentrations. These results suggest the existence of an inhibitory dopaminergic and a stimulatory α-adrenergic influence on GtH release in goldfish.

Effects of dopamine on gonadotropin release in female goldfish, Carassius auratus.

Intraperitoneal injections of dopamine (DA) or its agonist, apomorphine decreased and pimozide, a DA antagonist, increased serum gonadotropin (GtH) levels in normal female goldfish. Injection of DA into the third cranial ventricular did not alter serum GtH concentrations. Intraperitoneal injections of DA or apomorphine each reduced the highly elevated serum GtH levels caused by preoptic lesions which abolish an inhibitory hypothalamic influence on GtH release allowing prolonged spontaneous release of GtH. Intraperitoneal injections of DA or apomorphine blocked the stimulation of GtH release induced by injections of a luteinizing hormone-releasing hormone analogue. These results indicate that DA has GtH release-inhibitory activity by actions directly on gonadotrophs to inhibit spontaneous secretion of GtH, and by blocking the actions of the GtH-releasing hormone.