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Biomedical subjects

R E Peter

Publications and source records attributed to R E Peter.

At least 109 records · Page 6Linked to original sources
PubMed1991

Demonstration of gonadotropin releasing-hormone receptors on gonadotrophs and somatotrophs of the goldfish: an electron microscope study.

Dispersed pituitary cells of the goldfish were incubated with biotinylated [D-Lys6, Pro9-N-ethylamide] salmon gonadotropin-releasing hormone (sGnRH-A) then avidingold (10 nm), and were fixed, embedded and sectioned. Cells were identified as gonadotrophs, somatotrophs, or prolactin cells using specific hormone antisera and protein-A gold (20 nm) as a marker. Attachment of the biotinylated sGnRH-A to the pituitary cell sections was determined by scanning cell surfaces for the smaller gold particles using the transmission electron microscope. Attachment was observed on gonadotrophs and somatotrophs, but was negligible on prolactin cells. Preincubation with unlabelled salmon gonadotropin-releasing hormone or chicken II gonadotropin-releasing hormone, or omission of the salmon gonadotropin-releasing hormone analog, prevented the reaction. The direct visualization of specific gonadotropin-releasing hormone receptors on gonadotrophs and somatotrophs supports the existence of direct stimulatory actions of gonadotropin-releasing hormone on gonadotropin and somatotropin release in gold-fish.

Animals↗
PubMed1991

In vitro release of gonadotropin-releasing hormone from the brain preoptic-anterior hypothalamic region and pituitary of female goldfish.

In vitro release of gonadotropin releasing hormone (GnRH) from slices of the preoptic-anterior hypothalamic (P-AH) region and fragments of the pituitary of goldfish was studied using a static incubation system. Release of GnRH from both tissue preparations was stimulated by depolarizing concentrations of extracellular potassium ions (K+). Other putative secretagogues, calcium ionophore A23187 (1 microM), forskolin (100 microM), and prostaglandin E2 1 microM) also stimulated release of GnRH from both tissue preparations. Omission of Ca2+, or chelating the remaining remaining Ca2+ by EGTA (0.1 mM), abolished the release of GnRH stimulated by high K+ concentrations (60 mM), but did not reduce spontaneous release. Verapamil (1 microM), a voltage-sensitive calcium channel blocker, abolished the release of GnRH stimulated by high K+ or A21387 from both tissue preparations. The GnRH released in vitro from both the P-AH region and pituitary was concentrated by Sep-Pak and then separated by high-performance liquid chromatography. The major peak of the GnRH immunoreactivity was found to coelute with synthetic salmon GnRH [( Trp7,Leu8]-GnRH) and the minor peak with chicken GnRH-II [( Gln8]-GnRH). Dopamine (10 and 100 microM) inhibited GnRH release from both P-AH slices and pituitary fragments, while serotonin (1-100 microM) stimulated release from both. Norepinephrine (10-100 microM) stimulated GnRH release from P-AH slices but not from pituitary fragments. The results demonstrate that the release of GnRH from goldfish P-AH slices and pituitary fragments in vitro in response to various secretagogues and monoamines can be studied using a static incubation system.

Amino Acid Sequence↗
PubMed1991

Isolation and characterization of a gonadotropin-releasing hormone binding protein in goldfish serum.

A binding protein (BP) specific for gonadotropin-releasing hormone (GnRH) was previously demonstrated in goldfish serum. In the present study the binding protein was isolated and further characterized. The GnRH-BP, partially purified from goldfish serum using polyacrylamide gel electrophoresis (PAGE) under nondenaturing conditions, was concentrated in a single band, separate from all major components of serum proteins. The binding ability of the partially purified GnRH-BP was conserved; the isolated GnRH-BP specifically bound salmon GnRH and chicken GnRH-II, the native forms of GnRH present in goldfish, but not other forms of GnRH. The relative binding affinity of the partially purified GnRH-BP was [D-Arg6,Pro9-NEt]-salmon GnRH greater than chicken GnRH-II greater than or equal to salmon GnRH. The GnRH-BP, in raw serum or partially purified by PAGE, was specifically covalently labeled using 125I-[D-Lys6,Pro9-NEt]-salmon GnRH and the bifunctional cross-linking reagent, disuccinimidyl suberate, and then subjected to sodium dodecyl sulfate-PAGE under reducing conditions. The location of the radiolabeled GnRH-BP on PAGE gels was determined by cutting gels into sections and counting the radioactivity, or by autoradiography; the molecular weight of the GnRH-BP was estimated to be 40 KD. The covalently labeled GnRH-BP extracted from SDS-PAGE was subjected to high pressure liquid chromatography, and it coeluted with a single protein peak of the GnRH-BP partially purified by PAGE under nonreducing conditions. These studies demonstrate that the GnRH-BP is a minor component of serum proteins in goldfish; it is a single nonglycoprotein of about 40 kDa.

Affinity Labels↗
PubMed1991

Metabolism of gonadotropin-releasing hormone in goldfish: serum clearance and tissue uptake studies.

The metabolic clearance rate (MCR) and initial half-disappearance time (T(1/2)i) of salmon gonadotropin-releasing hormone (sGnRH) and its agonist analog [D-Arg6,Pro9-NEt]-sGnRH (sGnRH-A) were investigated in goldfish, following a single intraarterial injection of radioiodinated sGnRH and sGnRH-A. The tissue uptake of radioiodinated sGnRH-A was also investigated. 125I-sGnRH had a MCR of 0.01173 ml min-1 35 g-1 and a (T(1/2)i) of 32.38 min; 125I-sGnRH-A had a MCR of 0.0192 ml min-1 35 g-1 and a (T(1/2)i) of 72.95 min. In the tissue uptake experiments, high levels of accumulated labeled sGnRH-A were generally found in the gills, kidney, liver, and pituitary compared to air bladder, brain, gonad, eyes, and muscle. Coinjection of excess amount of cold sGnRH-A caused decreased uptake of labeled sGnRH-A only in pituitary, but increased accumulation of labeled sGnRH-A in some other tissues. Our results show a correlation between the T(1/2)i and the affinity of the peptides for a serum GnRH binding protein present in the goldfish, suggesting that the formation of a hormone-binding protein complex may decrease the MCR of GnRH in the circulation in goldfish. Our data also indicate specific uptake of 125I-sGnRH-A by the pituitaries of both male and female goldfish, confirming the pituitary as a major target organ of GnRH in goldfish.

Air Sacs↗
PubMed1991

Evaluation of a specific gonadotropin-releasing hormone binding protein in the serum of goldfish: a study on the influence of sex, season, GnRH injection and estradiol treatment in vivo.

A gonadotropin releasing hormone (GnRH) binding protein (GnRH-BP) from goldfish serum was isolated and characterized. In the present studies, the differences in serum titer of GnRH-BP between male and female goldfish, and between goldfish at different stages of gonadal development, were investigated. The effects of estradiol (E2) treatment or multiple injections of [D-Arg6-Pro9-NEt]-salmon GnRH (sGnRH-A) treatment on the serum titer of GnRH-BP were also studied. GnRH-BP in individual serum samples was quantified with a ligand binding assay using 125I-sGnRH-A as tracer; GnRH-BP-tracer complex was separated from free tracer by gel filtration using Sephadex G-50 mini-columns. GnRH-BP was detected in every individual sample; however, no differences between males and females, nor seasonal changes in either sex, were detected. Serum total protein content doubled with E2 treatment, but no effects of E2 on GnRH-BP titer were detected. Long-term treatment with sGnRH-A stimulated an increase in serum gonadotropin levels; the long-term treatment with sGnRH-A did not alter the serum titer of GnRH-BP. Although the GnRH-BP is present in excess relative to the low concentration of GnRH in goldfish serum, it is not a major component of serum proteins. It is concluded that the serum titer of GnRH-BP was not fine tuned by GnRH, gonadotropin, or estradiol. Therefore physiological regulators have yet to be discovered.

Animals↗
PubMed1991

Effects of serotonin on gonadotropin and growth hormone release from in vitro perifused goldfish pituitary fragments.

The effects of serotonin (5-HT) on gonadotropin and growth hormone release from perifused goldfish (Carassius auratus, L.) pituitary glands were studied. Serotonin, at micromolar concentrations, caused a dose-related release of gonadotropin and an inhibition of growth hormone release in pituitaries from goldfish at different sexual stages. At lower concentrations 5-HT continued to inhibit growth hormone release, but had no effects on gonadotropin release. The stimulatory effects of 5-HT on gonadotropin release could be blocked by ketanserin and cyproheptadine; however, these two antagonists had no effects on 5-HT inhibition of growth hormone release. Perifusion with melatonin had no effect on the release of gonadotropin or growth hormone release. These results demonstrate that 5-HT has a stimulatory effect on gonadotropin secretion, probably through a 5-HT2 receptor type, and an inhibitory effect on growth hormone through an unidentified receptor type. We hypothesize that the effects on gonadotropin release are due to direct actions on gonadotrophs, whereas the effects on growth hormone release may be due to stimulation of somatostatin release from neurosecretory terminals in the pituitary.

Animals↗
PubMed1991

Testosterone and estradiol potentiate the serum gonadotropin response to gonadotropin-releasing hormone in goldfish.

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.

Animals↗
PubMed1991

External fixation of the sternum for thoracic trauma.

A flail chest with a manubriosternal separation in a man with multiple injuries was treated with an external fixator applied to the sternum and the manubrium. Pain and ventilatory function were improved, permitting immediate postoperative extubation and prompt patient mobilization. The external fixator was removed after fracture union at 2 months. One year after injury, the patient's pulmonary function was normal. External fixation is an alternative to other methods of sternal fracture stabilization.

Abdominal Injuries↗
PubMed1991

Carassin: a tachykinin that is structurally related to neuropeptide-gamma from the brain of the goldfish.

A 21-amino-acid residue tachykinin-related peptide, carassin, was isolated in pure form from an extract of the brain of the goldfish, Carrassius auratus, by reversed-phase HPLC. The primary structure of the peptide was established as the following: Ser-Pro-Ala-Asn-Ala-Gln-Ile-Thr-Arg-Lys-Arg-His-Lys-Ile-Asn- Ser-Phe-Val-Gly-Leu-Met.NH2. This amino acid sequence is the same length as and shows structural similarity (57% homology) to the mammalian tachykinin, neuropeptide-gamma, which is a product of the posttranslational processing of gamma-preprotachykinin. The mammalian tachykinins, substance P and neurokinin B, were not detected in the extract by using specific antisera directed against the NH2-termini of the peptides, but an antiserum directed against the COOH-terminal region of substance P did detect a low concentration of immunoreactive material.

Amino Acids↗
PubMed1991

Selective depletion of dopamine in the goldfish pituitary caused by domperidone.

The effects of the dopamine type-2 receptor (D-2) antagonist domperidone on pituitary and brain amine concentrations and serum gonadotropin levels in the goldfish were investigated. Domperidone caused a long-lasting, dose-dependent depletion of dopamine in the goldfish pituitary. Pituitary concentrations of 5-hydroxytryptamine (5HT) were unaffected by domperidone treatment. Concentrations of noradenaline, dopamine, and 5HT in the hypothalamus and telencephalon were also unaffected by domperidone treatment. In contrast to the goldfish, dopamine levels in both mouse pituitary and hypothalamus were unaffected by domperidone treatment. The depletion of dopamine was observed in both sexually regressed and recrudescent, male and female fish, but elevation of serum gonadotropin levels in response to domperidone treatment occurred only in sexually recrudescent fish. Treatment of sexually recrudescent fish with the D-2 antagonists pimozide, (-)-sulpiride and eticlopride and the dopamine type-1 (D-1) antagonists SKF 83566 and SCH 23390 failed to elicit a depletion of pituitary dopamine or elevation of serum gonadotropin. Treatment of sexually recrudescent fish with domperidone, alpha-methyl-p-tyrosine or carbidopa elicited comparable depletions of pituitary dopamine and elevations of serum gonadotropin. The results suggest that in addition to D-2 receptor antagonist activity, domperidone has some other neuropharmacological action on dopaminergic neurones in the goldfish pituitary.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

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 F2 alpha (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 (lOTX) olfactory tract were carried out in male goldfish. Both OTX and mOTX, but not lOTX, 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.

Animals↗
PubMed1990

Growth hormone-dependent potentiation of gonadotropin-stimulated steroid production by ovarian follicles of the goldfish.

The possible involvement of growth hormone (GH) in the regulation of ovarian function in the goldfish was investigated by determining the effects of common carp GH on steroid production by vitellogenic and preovulatory ovarian follicles incubated in vitro. Carp GH acts in a dose-dependent manner to potentiate the actions of common carp gonadotropin (GtH) on the production of 17 beta-estradiol and testosterone by vitellogenic ovarian follicles and the actions of human chorionic gonadotropin (hCG) on testosterone production by preovulatory ovarian follicles. Carp GH alone had no effect on basal steroid secretion by either class of ovarian follicles. Chum salmon GH but not bovine GH also enhanced carp GtH-induced production of 17 beta-estradiol by vitellogenic ovarian follicles. Common carp prolactin had no effects on basal or GtH-stimulated steroid production by vitellogenic or preovulatory ovarian follicles. The actions of carp GH on preovulatory follicles were not apparent when tested with the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, suggesting that GH may act to enhance either the formation or actions of cAMP. In summary, these data demonstrate that GH has a direct modulatory effect on GtH-stimulated steroid production and suggest that GH may be an important regulator of follicular development in the goldfish.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Characterization of dopamine D2 receptors in the pituitary of the African catfish, Clarias gariepinus.

Dopamine receptors in the pituitary of the African catfish, Clarias gariepinus, were characterized using [3H]spiperone as radioligand. Specific binding of [3H]spiperone to pituitary membranes reached equilibrium within 60 min of incubation. The binding of the radioligand was tissue specific since the amount of binding was linear with pituitary membrane content in the incubations. In addition, pituitary membranes were observed to bind considerably more [3H]spiperone, compared to membrane preparation of various other tissues. Saturation experiments revealed the presence of a single class of high affinity/low capacity binding sites. The binding characteristics, estimated by Scatchard analysis, were: Kd = 3.2 +/- 0.5 x 10(-9) M and Bmax = 105 +/- 5 fmol/mg protein. Specific binding was displaceable with dopamine and with various specific D2 agonists and antagonists. The nature of displacement curves resembles those observed in studies on mammalian dopamine receptors. Binding experiments with cell fractions, obtained after centrifugation of dispersed pituitary cells over a Percoll density gradient, showed that most [3H]spiperone binding was obtained in an enriched gonadotropic cell fraction. This observation indicates that the receptor characteristics, estimated with the [3H]spiperone assay, are representative for dopamine receptors on the gonadotropic cells.

Animals↗
PubMed1990

Seasonal changes in serum gonadotropin, testosterone, 11-ketotestosterone, and estradiol-17 beta levels and their relation to tumor burden in gonadal tumor-bearing carp x 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 gonadotropic 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- and ketotestosterone (11-KT), and estradiol-17 beta (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.

Animals↗
PubMed1990

Use of a pituitary cell dispersion method and primary culture system for the studies of gonadotropin-releasing hormone action in the goldfish, Carassius auratus. I. Initial morphological, static, and cell column perifusion studies.

Two cell dispersion methods for excised goldfish pituitary glands were tested, and a cultured dispersed cell system based on trypsin enzymatic tissue digestion was developed and characterized. Controlled trypsin/DNase treatment of goldfish pituitary gland yielded dispersed cells of high viability (trypsin blue exclusion test) that responded to gonadotropin (GTH)-releasing hormone (GnRH) challenges with GTH secretion in a time- and dose-dependent manner following overnight culture. Electron microscopy revealed that cell preparations produced by the trypsin dispersion were free of cell debris and nerve terminals. The dispersed pituitary cells also retained distinct morphological and immunological identities. Under static incubation conditions, 2-hr treatments with 0.1 nM to 1 microM [Trp7,Leu8]-GnRH (sGnRH) and [D-Arg6,Pro9-N-ethylamide]-sGnRH (sGnRHa) stimulated GTH release with similar efficacy, but with ED50S of 1.92 +/- 0.48 and 0.19 +/- 0.08 nM, respectively. [His5,Trp7,Tyr8]-GnRH (cGnRH-II) stimulated GTH release in a nonsigmoidal, but dose-dependent manner, and with a higher efficacy than sGnRH. In contrast, sGnRH, sGnRHa, and cGnRH-II were equipotent in inducing growth hormone (GH) secretion in static culture studies and with ED50S of 0.29 +/- 0.13, 0.18 +/- 0.11, and 0.19 +/- 0.17 nM, respectively. When trypsin/DNase-dispersed cells cultured overnight with cytodex beads were tested in a cell column perifusion system, dose-related increase in GTH secretion, as well as GH release, were also observed with 0.5 to 50 nM sGnRH. These results suggest that trypsin-dispersed goldfish pituitary cells can be used effectively to study the actions of GnRH on teleost pituitary either in short-term static incubation or column perifusion studies. Differences in the GTH and GH responses to the two native GnRH forms, sGnRH and cGnRH-II, are also indicated.

Animals↗
PubMed1990

Photoaffinity labeling of pituitary gonadotropin-releasing hormone receptors in goldfish (Carassius auratus).

Receptors for GnRH were labeled by use of an iodinated (125I) photoreactive GnRH derivative [D-Lys6-azidobenzoyl]-GnRH. This derivative was found to bind to two classes of GnRH binding sites: high-affinity/low-capacity sites and low-affinity/high-capacity sites. The binding affinity of [D-Lys6-azidobenzoyl]-GnRH was found to be greater than that of D-Lys6-GnRH, but lower than a superactive fish GnRH agonist [D-Arg6, Trp7, Leu8, Pro9-NEt]-GnRH (sGnRH-A). Analysis of the photoaffinity-labeled goldfish pituitary GnRH receptors by SDS-PAGE and autoradiography indicated the presence of three labeled proteins displaceable by unlabeled sGnRH-A. The first and the most prominently labeled band was a 71,000-Mr protein, the second a 51,000-Mr protein, and the third a minor band of 130,000 Mr. Displacement characteristics of the 71,000- and 130,000-Mr bands were consistent with those of the low-affinity binding sites; displacement of the iodinated ligand from these proteins was achieved only in the presence of 10(-6) M sGnRH-A. The 51,000-Mr band had characteristics similar to those of the high-affinity site; displacement of the labeled ligand was achieved in the presence of 10(-9) M sGnRH-A. These findings provide for the first time some biochemical characterizations of pituitary GnRH receptors in a nonmammalian vertebrate.

Affinity Labels↗
PubMed1990

Differential actions of dopamine receptor subtypes on gonadotropin and growth hormone release in vitro in goldfish.

Incubation of cultured goldfish pituitary cells with 10 nM to 1 microM apomorphine (APO), a non-selective dopamine agonist, increased growth hormone (GH) release in a dose-dependent manner. GH release was also stimulated in a dose-dependent manner by 0.1 nM to 1 microM salmon gonadotropin (GTH)-releasing hormone (sGnRH), sGnRH analog, and chicken GnRH-II (cGnRH-II). The magnitude of GH responses to 1 microM GnRHs were less than that to 1 microM APO. GH responses to 10 nM to 1 microM APO were not significantly increased by the addition of GnRHs. Static incubations with 0.1 nM to 1 microM of the dopamine D1 agonist SKF38393 did not alter basal GTH release, or the GTH responses to 10 nM sGnRH and cGnRH-II. In contrast, the D1 agonist SKF38393 significantly increased basal GH secretion with maximal stimulation achieved at 100 nM concentration, and GH responses to 10 nM sGnRH and 10 nM cGnRH-II were enhanced by simultaneous applications of SKF38393. Incubation with 1 microM of the D2 agonist LY171555 decreased basal GTH release. Additions of 0.1 nM to 1 microM LY171555 caused dose-dependent decreases in the GTH secretion induced by 10 nM sGnRH and cGnRH-II. In contrast, basal and GnRH-stimulated GH release were not affected by coincubations with LY171555. The D1 antagonist SKF83566 and the D2 antagonist domperidone, at 1 microM concentrations, specifically blocked the D1 agonist SKF38393-stimulated increase in GH release and the D2 agonist LY171555-induced depression of GTH secretion, respectively. In cell column perifusion studies, the D1 agonist SKF38393 at 0.1 nM to 1 microM had no effects on GTH release, but significantly elevated GH secretion rates when applied at 0.1-1 microM concentrations. The GH release induced by 1 microM SKF38393 was significantly reduced by simultaneous perifusion with 1 microM of the D1 antagonist SKF83566. Treatments with SKF38393 and/or SKF83566 did not affect net GTH and GH responses to sGnRH challenges. In contrast, perifusion with 0.1 and 1 microM of the D2 agonist LY171555 depressed basal as well as sGnRH-induced GTH responses. These effects of 1 microM LY171555 were completely blocked by simultaneous applications of 1 microM domperidone, a D2 antagonist. Treatments with these D2 selective drugs did not affect basal and sGnRH-stimulated GH release. These results indicate that in cultured goldfish pituitary cells, activation of dopamine D1- and D2-like receptors specifically stimulates GH release and inhibits both basal and stimulated GTH secretion, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗