Biomedical subjects

R E Peter

Publications and source records attributed to R E Peter.

At least 91 records · Page 5Linked to original sources

PubMed1993

In vitro and in vivo evidence that dopamine exerts growth hormone-releasing activity in goldfish.

We have previously demonstrated that dopamine (DA) and the DA D1 agonist SKF 38393 stimulate growth hormone (GH) release from perifused pituitary fragments of the goldfish, suggesting an involvement of DA D1 receptors in GH regulation. In the present study, the role of DA on GH release and body growth of the goldfish was further investigated both in vivo and in vitro. DA consistently stimulated GH release in a dose-dependent manner from perifused goldfish pituitary fragments. The GH-releasing action of DA was seasonal, being the highest in sexually regressed fish, intermediate in recrudescent fish, and the lowest in sexually mature (prespawning) fish. Somatostatin, a known GH-release inhibitor in the goldfish, suppressed basal GH release and abolished the GH response to DA in perifused pituitary fragments as well as pituitary cells under static incubation. Intraperitoneal administration of the nonselective DA agonist apomorphine and the D1 agonist SKF 82958 increased the plasma GH levels in the goldfish. These GH responses were blocked by simultaneous treatment with the D1 antagonist Sch 23390 but not the D2 antagonist pimozide. Apomorphine administered orally also induced a similar elevation in plasma GH levels. Long-term feeding with apomorphine was found to be stimulatory to the body growth of goldfish. These results provide evidence that the neurotransmitter DA, by acting through DA D1 receptors in the pituitary, also functions as a GH-releasing factor in the goldfish.

Administration, Oral↗

PubMed1993

GABA stimulation of gonadotropin-II release in goldfish: involvement of GABAA receptors, dopamine, and sex steroids.

The involvement of gamma-aminobutyric acid (GABA) in regulation of pituitary gonadotropin-II (GTH-II) release was studied in the goldfish. Intraperitoneal injection of GABA (300 micrograms/g) stimulated an increase in serum GTH-II levels at 30 min postinjection. The GABAA receptor agonist muscimol (0.1-10 micrograms/g) stimulated GTH-II in a dose-dependent manner. Baclofen, a GABAB receptor agonist, had a small but significant stimulatory effect at 1 and 10 micrograms/g; the amount of GTH-II released in response to baclofen was significantly less (P < 0.05) than that released by muscimol. Pretreatment of goldfish with bicuculline, a GABAA receptor antagonist, but not saclofen, a GABAB receptor antagonist, blocked the stimulatory effect of GABA on serum GTH-II. Elevation of brain and pituitary GABA levels with the GABA transaminase inhibitor, gamma-vinyl-GABA (GVG), decreased hypothalamic and pituitary dopamine (DA) turnover rates, indicating that GABA may stimulate GTH-II release in the goldfish by decreasing dopaminergic inhibition of GTH-II release. The release of GTH-II stimulated by muscimol and GVG was potentiated by pharmacological agents that decrease inhibitory dopaminergic tone, indicating that DA may also inhibit GABA-stimulated GTH-II release. Based on the linear 24-h accumulation of GABA in brain and pituitary after GVG injection, implantation of testosterone, estradiol, or progesterone, previously shown to regulate the serum GTH-II release response to gonadotropin-releasing hormone and GABA, was also found to modulate GABA synthesis in the brain and pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminocaproates↗

PubMed1993

Neuropeptide-Y stimulates growth hormone and gonadotropin-II secretion in the goldfish pituitary: involvement of both presynaptic and pituitary cell actions.

We have previously reported that neuropeptide-Y (NPY) stimulates GH and gonadotropin-II (GtH-II) release from perifused pituitary fragments in the goldfish. Since the teleost pituitary is directly innervated by neurosecretory terminals from the brain, we further investigated the possible sites of action of NPY. Both synthetic human NPY and NPY-(18-36), an agonist selective for the NPY Y2-receptor, stimulated GH and GtH-II release from the pituitary fragments; the magnitude of the response to NPY (18-36) was smaller than that to the whole molecule of NPY. NPY also stimulated the release of GH and GtH-II from perifused dispersed pituitary cells. In contrast, NPY-(18-36) had no effect on either GH or GtH-II release from dispersed pituitary cells. These data suggest that Y2 action is not direct at the level of pituitary cells, but may be indirect through actions on nerve terminals in the pituitary. The hypothesis that the action of NPY on GH and GtH-II release is mediated in part by GnRH was then tested. Both NPY and NPY-(18-36) stimulated the GnRH release from preoptic-anterior hypothalamic slices and pituitary fragments with similar potency. Furthermore, a GnRH antagonist significantly reduced the effects of NPY on both GH and GtH-II release in perifused pituitary fragments. Similar to previous findings, NPY, when given at 55-min intervals, desensitized the hormone responses in pituitary fragments. Similarly, the same treatment with NPY in perifused dispersed pituitary cells induced desensitization of GH and GtH-II responses. Together, these results suggest that 1) more than one type of NPY receptors are present in the goldfish pituitary; and 2) NPY has at least two sites of action in the pituitary. One site of action is the pituitary cells, where NPY directly stimulates GH and GtH-II secretion; the second is the nerve terminals, where NPY presynaptically stimulates GnRH release via Y2-like receptors, and GnRH, in turn, stimulates GH and GtH-II release.

Animals↗

PubMed1993

Characterization of D1 receptors mediating dopamine-stimulated growth hormone release from pituitary cells of the goldfish, Carassius auratus.

Previously, we demonstrated that dopamine (DA) stimulates GH release from the pituitary of goldfish, and this action is mediated by D1-like receptors. In the current study, we have provided evidence for the presence of D1-specific binding sites in the pituitary cells of goldfish. These D1-binding sites were found to be saturable, stereospecific, and selective for D1 ligands. The rank order of binding affinity of these D1-binding sites is (+)SCH23390 > SKF83566 >> (-)SCH23390 > domperidone > LY171555 >> serotonin. The association of these D1-binding sites with [3H]SCH23390, a D1-specific radioligand, was rapid, reversible, and exhibited a high binding affinity in the nanomolar range. The Kd values were estimated to be 33.7 +/- 8.5 nM for mixed populations of pituitary cells and 10.9 +/- 2.5 nM for pituitary cell preparations enriched with somatotrophs. Autoradiographic studies revealed that specific binding of [3H]SCH23390 was predominantly localized in the pars distalis, not in the neurointermediate lobe of the goldfish pituitary. Furthermore, these D1-binding sites in the goldfish pituitary cells could be functionally correlated with the GH-releasing actions of DA. Since these D1-binding sites exhibited the expected pharmacological properties of mammalian D1 receptors, we conclude that DA D1 receptors are present in the goldfish pituitary and are responsible for the mediation of DA D1-stimulated GH release. The apparent similarities of the D1 receptor pharmacology between goldfish and mammals also suggests that DA D1 receptors are highly conserved during vertebrate evolution.

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

PubMed1993

In vitro characterization of gonadotropin-releasing hormone antagonists in goldfish, Carassius auratus.

The two native forms of GnRH, salmon GnRH and chicken GnRH-II, in the brain and pituitary of goldfish are both active in stimulating gonadotropin-II (GTH-II) and GH release. The objective of the present study was to characterize GnRH antagonists for their ability to inhibit sGnRH- and cGnRH-II-induced GTH-II and GH release in goldfish using a pituitary fragments perifusion system. Contrary to expectations, putative GnRH antagonists with D-Arg6 stimulated GTH-II and GH release in nearly all cases. [Ac-delta 3-Pro1,4FD-Phe2,D-Trp3,6]mammalian (m) GnRH inhibited sGnRH- and cGnRH-II-stimulated GTH-II release in a dose-dependent manner, with ED50 values of 242 +/- 48 and 169 +/- 17 nM, respectively. [Ac-delta 3-Pro1,4FD-Phe2,D-Trp3,6]mGnRH also inhibited GH release stimulated by sGnRH (ED50, 128 +/- 74 nM) and cGnRH-II (ED50, 157 +/- 67 nM). The degree of inhibition was higher in sexually regressed fish compared to postspawning fish. [D-p-Glu1,D-Phe2,D-Trp3,6]mGnRH suppressed both sGnRH- and cGnRH-II-induced GTH-II release with ED50 values of 326 +/- 96 and 249 +/- 74 nM, respectively. [Ac-delta 3-Pro1,4FD-Phe2,D-Trp3,6]sGnRH inhibited sGnRH and cGnRH-II stimulated GTH-II release, but stimulated GH release. On the other hand, [Ac-D(2)-Nal1,4Cl-D-Phe2,D-(3)Pal3,6,Arg5,D-A la10]mGnRH weakly stimulated GTH-II release, but strongly inhibited basal GH release. These results indicate that [Ac-delta 3-Pro1,4FD-Phe2,D-Trp3,6]mGnRH has clear antagonistic activity on sGnRH and cGnRH-II stimulation of GTH-II and GH release in vitro. The differential actions of a few GnRH analogs on GTH-II and GH release indicate that the properties of the GnRH receptors on GTH and GH cells may be different. The amino acid in position 6 plays an important role in determining the nature of intrinsic activity of GnRH peptides, and substitution of D-Arg6 normally produces agonistic analogs.

Amino Acid Sequence↗

PubMed1993

[Fracture of the femoral neck: therapeutic approach].

The therapeutic approach for treatment of femoral neck fractures is reviewed. The choice of implant is dependent primarily on patient age and amount of fracture displacement. Hemiarthroplasty remains the treatment of choice for displaced femoral neck fractures in older or debilitated patients. Internal fixation is always indicated in healthy and active subjects, whether the fracture is displaced or undisplaced. Internal fixation with three cancellous screws provides good mechanical stability without compromising head vitality when compared to other implants.

Adult↗

PubMed1992

Distinct sequence of gonadotropin-releasing hormone (GnRH) in dogfish brain provides insight into GnRH evolution.

In vertebrates, gonadotropin-releasing hormone (GnRH) belongs to a family of decapeptides characterized by the conservation of residues 1, 2, 4, 9, and 10. In the jawed vertebrates only positions 5, 7, and 8 in the GnRH molecules vary. We have now purified two forms of GnRH from the brains of spiny dogfish (Squalus acanthias) by using reverse-phase high-performance liquid chromatography. The primary structures were established by automated Edman degradation and mass spectral analysis. The distinct structure of the first form (dogfish GnRH) is pGlu-His-Trp-Ser-His-Gly-Trp-Leu-Pro-Gly-NH2 (pGlu represents pyroglutamyl). The second peptide is identical to a form of GnRH originally isolated from chicken brains (chicken GnRH-II; pGlu-His-Trp-Ser-His-Gly-Trp-Tyr- Pro-Gly-NH2) and is widespread throughout the vertebrates. We are aware of no other species of cartilaginous fish in which the primary structures of two forms of GnRH have been determined. The presence of chicken GnRH-II in dogfish supports the idea that chicken GnRH-II is the oldest GnRH to evolve in jawed vertebrates. With the addition of the dogfish GnRH structure to the family, two main structural branches of GnRH can be delineated. The physiological effects of dogfish GnRH included the release of not only gonadotropin but also growth hormone from goldfish pituitary fragments.

Amino Acid Sequence↗

PubMed1992

Activity of vertebrate gonadotropin-releasing hormones and analogs with variant amino acid residues in positions 5, 7 and 8 in the goldfish pituitary.

All non-mammalian vertebrates as well as marsupial mammals have two or more forms of gonadotropin-releasing hormone (GnRH) in the brain. Goldfish brain and pituitary contains two molecular forms of GnRH, salmon GnRH ([Trp7, Leu8]m-GnRH; s-GnRH) and chicken GnRH-II ([His5, Trp7, Tyr8]m-GnRH; cII-GnRH). Both sGnRH and cII-GnRH stimulate gonadotropin (GtH) as well as growth hormone (GH) release from the goldfish pituitary. The purpose of the present study was to study the activity of the five known forms of GnRHs as well as analogs of mammalian GnRH (m-GnRH) with variant amino acid residues in positions 5, 7 and 8 in terms of binding to GnRH receptors, and release of GTH and GH from the perifused fragments of goldfish pituitary in vitro. All five vertebrate GnRH peptides stimulated both GtH and GH release in a dose-dependent manner, although their potencies were very different. cII-GnRH was somewhat more active than s-GnRH in releasing GtH, whereas s-GnRH tended to have a greater potency than cII-GnRH in terms of GH release. Both chicken GnRH-I (cI-GnRH) and lamprey GnRH (l-GnRH) were significantly less potent than mGnRH, s-GnRH and cII-GnRH in releasing GtH and GH. cII-GnRH binds with higher affinity for the high affinity binding sites compared to all other native peptides. The activity of [Trp7]-GnRH was similar to both s-GnRH and cII-GnRH in releasing GtH and GH. Substitution of His5 resulted in a significant decrease in GtH releasing potencies compared to mGnRH, sGnRH and cII-GnRH. [His5]-GnRH also had lower GH releasing potency than mGnRH and sGnRH. Tyr8, His8 and Leu8 substitutions caused significant decreases in GtH releasing potencies compared to mGnRH, s-GnRH and cII-GnRH, but did not cause a significant change in GH releasing potency. The combination of [His5, Trp7]-GnRH had GtH and GH releasing activities similar to m-GnRH, s-GnRH and cII-GnRH.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗

PubMed1992

Properties of common carp gonadotropin I and gonadotropin II.

Two gonadotropins, GtH I and GtH II, were extracted with 35% ethanol-10% ammonium acetate, pH 6.1, from female common carp pituitary glands and purified by ion-exchange chromatography on a DE-52 column followed by gel filtration on a Sephadex G-75 column. Molecular weights of GtH I and GtH II as determined by SDS-PAGE were 45,000 and 35,000, respectively. Both GtHs dissociate into two subunits following reduction with beta-mercaptoethanol. These subunits contain different N-terminal amino acids (Tyr and Gly for GtH I; Tyr and Ser for GtH II). GtH I was acid stable and did not dissociate into subunits following treatment with 0.1% trifluoroacetic acid; GtH II readily dissociated into subunits by this treatment. GtH I and GtH II have distinct elution profiles on reverse-phase HPLC. The N-terminal amino acid sequence of the beta-subunit of GtH II was identical to that of common carp maturational GtH described by other workers suggesting that GtH I is a newly identified molecule. This was supported by radioimmunoassay analysis. GtH II and a common carp maturational GtH preparation (F11 cGtH; Peter et al., 1982, J. Interdiscipl. Cycle Res. 13, 229-239) had similar immunological activity in tests with antisera to the beta-subunit of maturational GtH whereas GtH I had low (less than 6%) cross-reactivity. GtH I, GtH II, and F11 cGtH were equipotent in tests with antisera to the alpha-subunit of maturational GtH suggesting these molecules contain a similar alpha-subunit. In vitro bioassays using goldfish revealed that GtH I and GtH II share the same spectrum of biological activities causing stimulation of ovarian and testicular steroidogenesis and induction of oocyte final maturation. The demonstration of two chemically distinct GtHs in common carp is similar to what has been described for chum and coho salmon.

Amino Acid Sequence↗

PubMed1992

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

In goldfish, the gonadal steroid, 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-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 17,20 beta-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 17,20 beta-P. Water-borne 17,20 beta-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 17,20 beta-P causes an abatement of DA release to the pituitary. Based on the latency of the GtH response to water-borne 17,20 beta-P, a rapid reduction of DA turnover in the pituitary appears to be at least part of the neuroendocrine trigger for 17,20 beta-P-induced GtH release in male goldfish.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Adrenergic and dopaminergic regulation of gonadotropin-releasing hormone release from goldfish preoptic-anterior hypothalamus and pituitary in vitro.

The involvement of adrenergic and dopaminergic receptor subtypes on in vitro release of radioimmunoassayable gonadotropin-releasing hormone (GnRH) from incubated preoptic-anterior hypothalamic (P-AH) slices and pituitary fragments of sexually mature male goldfish was studied. Norepinephrine (NE) produced a dose-related stimulation of GnRH from P-AH slices, but not from pituitary fragments. The effects of some adrenergic receptor agonists (1 microM) on GnRH release from P-AH slices were tested: phenylephrine (alpha 1-agonist) significantly stimulated GnRH release; clonidine (alpha 2-agonist) and isoproterenol (beta-agonist) were ineffective. Incubation of P-AH slices with phentolamine (alpha 1/alpha 2-antagonist) and prazosin (alpha 1-antagonist), at a concentration of 1 microM, inhibited the release of GnRH induced by NE (60 microM); the alpha 2-antagonist yombibin and the beta-antagonist propanolol were ineffective. None of the adrenergic antagonists (1 microM) tested produced significant effects on spontaneous release of GnRH from both tissue preparations. Spontaneous release of GnRH from both P-AH slices and pituitary fragments was reduced by dopamine (DA) in a dose-related manner. The effects of some DA agonists (1 microM) were tested: apomorphine (D1/D2-agonist) and SKF 38398 (D1-agonist), but not bromocriptine and LY-171555 (D2-agonists) significantly reduced spontaneous GnRH release from P-AH slices in vitro. On the other hand, D2-agonists, but not D1-agonists, significantly reduced GnRH release from pituitary fragments. The effects of DA antagonists (1 microM) were also tested: in P-AH slices, addition of SKF-83566 (D1-antagonist) significantly reduced spontaneous GnRH release; pimozide and domperidone (D2-antagonist) were ineffective when tested alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1992

Amino acid neurotransmitters and dopamine in brain and pituitary of the goldfish: involvement in the regulation of gonadotropin secretion.

An isocratic high-performance liquid chromatographic technique was developed to measure levels of gamma-aminobutyric acid (GABA), glutamate, and taurine in the brain and pituitary of goldfish. Accuracy of this procedure for quantification of these compounds was established by evaluating anesthetic and postmortem effects and by selectively manipulating GABA concentrations by intraperitoneal administration of the glutamic acid decarboxylase (GAD) inhibitor 3-mercaptopropionic acid or the GABA transaminase inhibitor gamma-vinyl GABA. The technique provided a simple, rapid, and reliable method for evaluating the concentrations of these amino acids without the use of complex gradient chromatographic systems. To investigate the relationship between neurotransmitter amino acids and the control of pituitary secretion of gonadotropin, the effects of injection of taurine, GABA, or monosodium glutamate on GABA, glutamate, taurine, and, in some instances, monoamine concentrations in the brain and pituitary were evaluated and related to serum gonadotropin levels. Injection of taurine caused an elevation in serum gonadotropin concentrations. In addition, injection of the taurine precursor hypotaurine but not the taurine catabolite isethionic acid elevated serum gonadotropin levels. Intracerebroventricular injection of either GABA or taurine also elevated serum gonadotropin concentrations. Pretreatment of recrudescent fish with alpha-methyl-p-tyrosine reduced pituitary dopamine concentrations and also potentiated the serum gonadotropin response to taurine. Injection of monosodium glutamate caused an increase of glutamate content in the pituitary at 24 h; this was followed by a decrease at 72 h after administration. Pituitary GABA, taurine, and dopamine concentrations underwent a transient depletion after monosodium glutamate administration, and this was associated with an elevation of serum gonadotropin content.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Mercaptopropionic Acid↗

PubMed1992

Influence of GABA on gonadotrophin release in the goldfish.

The influence of GABA on pituitary gonadotrophin (GTH) release in the goldfish was studied by means of in vivo and in vitro techniques. It was found that GABA injected intraperitoneally caused an increase of serum GTH levels in regressed or early maturing fish, but not in late maturing animals. Moreover, injection of a GABA transaminase inhibitor caused a significant increase of GABA within the hypothalamus and pituitary, and a dose-dependent increase in serum GTH levels. To determine if this effect could be exerted directly at the level of the pituitary, dispersed pituitary cells in static incubation or in perifusion were exposed to increasing concentrations of GABA or its agonists muscimol and baclofen. None of these drugs was able to modify the spontaneous or GnRH-induced secretion of GTH, indicating that the in vivo effect of GABA was most likely mediated via another hypothalamic factor. Using in vitro incubation of pituitary slices, it was found that GABA caused a dose-related stimulation of GnRH release at the level of the pituitary, providing a possible explanation for the observed in vivo stimulatory effect of GABA on GTH release. Since the seasonal effect of GABA in vivo indicated a possible interaction of GABA with sexual steroids, GABA was given intraperitoneally to female goldfish implanted with either testosterone or estradiol. We found that the stimulatory effect of GABA on GTH release was abolished in estradiol-treated females but was still observed in testosterone-implanted fish. Moreover, estradiol but not testosterone caused a decrease of the GABA concentration within the telencephalon.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobutyrate Transaminase↗

PubMed1992

Interactions of estradiol with gonadotropin-releasing hormone and thyrotropin-releasing hormone in the control of growth hormone secretion in the goldfish.

The effects of testosterone (T) and estradiol (E2) on serum growth hormone (GH) concentrations were investigated throughout the seasonal reproductive cycle of the female goldfish. Gonad-intact female goldfish were implanted intraperitoneally for 5 days with silastic pellets containing no steroid (blank), T(100 micrograms/g) or E2 (25-100 micrograms/g). In blank-implanted females, seasonal variations in serum GH were evident; maximal serum GH levels were found in spring while minimal GH levels were found in summer and early autumn. Implantation of E2-containing silastic capsules stimulated increases (2-4 times control) in serum GH levels throughout the reproductive cycle. Implantation of T did not affect serum GH at any time of the year. One possible mechanism by which E2 could exert its effects may be through alteration of pituitary sensitivity to GH-releasing factors. The decapeptide salmon gonadotropin-releasing hormone (sGnRH) is found in the brain and pituitary of goldfish and stimulates gonadotropin (GTH) and GH secretion. In contrast, thyrotropin-releasing hormone (TRH) stimulates GH, but not GTH, release from pars distalis fragments obtained from sexually regressed (ED50 = 5.7 +/- 3.8 nM; August) or sexually mature (ED50 = 0.53 +/- 0.28 nM; March) fish; in vivo E2 treatment resulted in a 3-fold increase in the in vitro GH response to TRH. Furthermore, E2 treatment increased sGnRH-stimulated GH release by approximately 4-fold. These results demonstrate that E2 but not T stimulates GH secretion throughout the reproductive cycle of female goldfish. Furthermore, sGnRH and TRH stimulate GH release in a teleost, and these stimulatory responses are enhanced by physiological levels of E2.

Animals↗

PubMed1992

Isolation and characterization of hypothalamic growth-hormone releasing factor from common carp, Cyprinus carpio.

A growth hormone-releasing factor (GRF)-like peptide was isolated from the hypothalamus of common carp, Cyprinus carpio, by acid extraction, gel filtration chromatography, immunoaffinity chromatography using antiserum directed against rat GRF, and multiple steps of HPLC using octadecyl columns. Based on Edman degradation and peptide mapping, this teleost GRF was established to be a 45-residue peptide with the following primary structure: His-Ala-Asp-Gly-Met-Phe-Asn-Lys-Ala-Tyr-Arg-Lys-Ala-Leu-Gly-Gln-Leu-Ser- Ala-Arg - Lys-Tyr-Leu-His-Thr-Leu-Met-Ala-Lys-Arg-Val-Gly-Gly-Gly-Ser-Met-Ile-Glu- Asp-Asp-Asn-Glu-Pro-Leu-Ser. Carp GRF is closely related structurally to peptides of the glucagon-secretin superfamily, and more particularly to mammalian vasoactive intestinal peptide (VIP) precursors and the N-terminal portion of mammalian GRFs. A synthetic replicate of this peptide is highly potent [50% effective dose (ED50) approximately 0.08 nM] in stimulating GH release from cultured goldfish pituitary glands and in elevating serum GH levels 30 min after injection (0.1 micrograms/g) in goldfish.

Amino Acid Sequence↗

PubMed1992

Dopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptors.

Previously, we have demonstrated that ip injection of apomorphine, a nonselective dopamine (DA) agonist, increases serum GH levels in the goldfish, suggesting a possible role of DA in GH regulation. In the present study, the effects of DA on GH release in the goldfish were further characterized using an in vitro perifusion system for pituitary fragments. DA increased GH release in a dose-dependent manner with an ED50 of 0.26 +/- 0.06 microM. SKF38393, a DA D1 agonist, mimicked the GH-releasing effect of DA with an ED50 of 0.41 +/- 0.12 microM. Stereoselectivity consistent with mammalian DA D1 systems was demonstrated for the GH response to SKF38393; only the (+)- but not (-)-enantiomer of SKF38393 induced a dose-dependent GH release. Two other D1 agonists, SKF77434 and SKF82958, were also found to have GH-releasing activity. In contrast, high doses (up to 1 microM) of the DA D2 agonists, bromocriptine and LY171555, did not affect basal GH levels. The receptor specificity for DA-stimulated GH release was further investigated by using D1 and D2 antagonists; the D1 antagonists SCH23390 and SKF83566 completely abolished the GH response to DA or the D1 agonist SKF38393, whereas the D2-specific antagonists domperidone and (-)-sulpiride were not effective in this respect. Taken together, the present study demonstrates that DA is stimulatory to GH release from the pituitary of goldfish, and its action is mediated through receptors resembling the mammalian DA D1 receptors. The apparent similarities of the DA D1 receptor pharmacology between the goldfish and the mammals also indicate that D1 receptor is highly conserved during vertebrate evolution.

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

PubMed1992

Effects of porcine follicular fluid, inhibin-A, and activin-A on goldfish gonadotropin release in vitro.

Inhibin and activin are important reproductive regulators in mammalian species and have been demonstrated to be highly conserved in structure. The present study examines the effects of porcine follicular fluid (pFF; a crude inhibin and activin preparation) and purified porcine inhibin-A and activin-A on goldfish gonadotropin-II (GTH-II) release. In studies using primary cultures of dispersed goldfish pituitary cells in static incubation, treatments with pFF, inhibin-A, and activin-A for 10 h caused dose-dependent increase in GTH-II release. In perifusion studies using goldfish pituitary fragments, basal GTH-II release was significantly elevated after 12-h exposure to 500 micrograms/ml pFF. Furthermore, GnRH-induced GTH-II secretion was potentiated by pretreatment with pFF. When pFF was applied in the form of 5-min pulses, a rapid dose-related stimulation of GTH-II was observed. Similarly, challenges with 2-min pulses of 15, 150, and 1500 pM inhibin-A and activin-A stimulated GTH-II release by goldfish pituitary fragments in a rapid and dose-dependent manner. This acute stimulatory action of inhibin on goldfish GTH-II release was completely abolished after pretreatment with specific inhibin antibodies. The acute actions of inhibin and activin on GTH-II release are probably not due to the release of endogenous GnRH from nerve terminals in the pituitary fragments or binding to the GnRH receptors. First, a specific GnRH antagonist did not block the actions of inhibin and activin. Second, dopamine, a potent inhibitor of GnRH-stimulated GTH-II secretion in goldfish, was only partially effective in decreasing inhibin- and activin-induced GTH-II release. Third, the stimulatory effects of inhibin and GnRH on GTH-II release were additive. These lines of evidence also indicate that the mechanisms mediating inhibin and activin stimulation of goldfish GTH-II release may be somewhat different from those of GnRH. These results demonstrate that in contrast with the usual inhibitory effects of inhibin on GTH release in mammals, both inhibin and activin exert long term and acute stimulatory actions on GTH-II release in the goldfish.

Activins↗

PubMed1992

Treatment of humeral diaphyseal fractures with Hackethal stacked nailing: a report of 33 cases.

Hackethal's technique of stacked intramedullary (IM) nailing was used to treat 43 consecutive acute fractures of the humeral diaphysis. Of these, 6 were lost to follow-up and 4 additional patients were excluded for pathologic fractures. All of the remaining 33 traumatic fractures were followed until union. The average age was 34 years. Mean operative time was 90 min. Usually four or five 2- or 3-mm IM Kirschner wires were introduced in a retrograde manner, through a posterior unicortical window under radioscopic control. Closed reductions were performed in 28 patients, and open reductions were performed in the other five. Time to follow-up averaged 3 years 5 months (range 8 months to 13 years). There were no infections. There were three nonunions (9%), and two nails in 1 patient penetrated the greater tuberosity and one nail migrated distally in another patient. This method of internal fixation is not complicated and causes minimal trauma. It provides good stability at the fracture site and permits early mobilization of patients with excellent functional results.

Adolescent↗