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Biomedical subjects

R E Peter

Publications and source records attributed to R E Peter.

At least 127 records · Page 7Linked to original sources

Neuropeptide Y stimulates growth hormone and gonadotropin release from the goldfish pituitary in vitro.

The effects of neuropeptide Y (NPY) on release of growth hormone (GH) and gonadotropin (GTH) from the goldfish pituitary in vitro were investigated. Exposure of perifused pituitary fragments, taken from female goldfish at late stages of gonadal recrudescence, to 5-min pulses of human NPY resulted in a rapid dose-dependent stimulation of GH and GTH release, with half-maximal effective dosages of 0.51 +/- 0.24 and 2.37 +/- 1.05 nM for GH and GTH, respectively. Repeated treatments with pulses of NPY (10 nM for GH, 5 nM for GTH) at 55-min intervals did not significantly alter the responsiveness of pituitary fragments to NPY; however, prior exposure of pituitary fragments to pulses of higher doses of NPY (50 nM GH, 10 nM for GTH) significantly reduced the subsequent hormone responses. When given at 85-min intervals repeated treatment with NPY did not blunt hormone responses to the second and third stimulations at these higher dosages. These results indicate that NPY acts at the pituitary level to stimulate GH and GTH secretion in female goldfish. The GTH response and, to a lesser extent, the GH response become desensitized to further stimulation by NPY in dose- and time-dependent manners. NPY should be considered as one element in the multifactorial systems regulating the GH and GTH secretion in goldfish.

Animals↗

Dopaminergic regulation of brain gonadotropin-releasing hormone in male goldfish during spawning behavior.

Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) concentrations in discrete brain areas of male goldfish was studied using the centrally active dopaminergic agonist apomorphine and antagonist pimozide. Pimozide caused time- and dose-dependent increases in serum gonadotropin levels and accumulation of GnRH in the olfactory bulbs, telencephalon and pituitary. The effects of pimozide were partially antagonized by apomorphine, which, when given alone, did not influence basal levels of brain GnRH and serum gonadotropin, but inhibited the increases in brain GnRH and serum gonadotropin levels that normally occur in response to spawning stimuli from prostaglandin-treated females. To study the physiological significance of the accumulation of brain GnRH due to central dopaminergic receptor blockade, the influences of pimozide on the brain GnRH and serum gonadotropin responses of male goldfish to spawning stimuli were tested. Pimozide pretreatment potentiated the serum gonadotropin increases and caused a marked reduction in the GnRH levels in olfactory bulbs, telencephalon and pituitary in response to spawning stimuli. These findings demonstrate that the central dopaminergic system is an important inhibitory component in the regulatory circuitry of brain GnRH levels in normal and behaviorally stimulated male goldfish.

Animals↗

Effect of a teleost GnRH analog on steroidogenesis by the follicle-enclosed goldfish oocytes, in vitro.

The influence of an agonist analog of teleost GnRH [(D-Arg6, Trp7, Leu8, Pro9-NEt)-GnRH; tGnRH-A] on steroidogenesis was studied in prophase-I arrested, follicle-enclosed, goldfish oocytes in vitro. Incubation of the follicles with carp gonadotropin (GtH) significantly increased production of 17 alpha-hydroxyprogesterone (HP) and testosterone following 24 hr of incubation in vitro. Concomitant incubation with tGnRH-A (10(-7) M) significantly attenuated the dose-related increase in GtH-induced testosterone production, but was without effect on the GtH-induced HP level. Time course studies indicated that tGnRH-A exerted its maximum inhibitory action on the GtH-induced testosterone production during the initial 8 hr of incubation in vitro. The inhibition of GtH-induced testosterone production by tGnRH-A was dose dependent with an ED50 of 1.39 +/- 2.88 nM. A significantly higher testosterone level was obtained in the incubation media containing HP as substrate; concomitant treatment with tGnRH-A reduced the conversion of HP to testosterone. The incubation media also contained low, but measurable levels of 17 alpha-hydroxy-20 beta-dihydroprogesterone (DHP), which increased in the presence of 3-isobutyl-methyl-xanthine; lower levels of DHP were obtained in the groups incubated with tGnRH-A. In view of our present findings and previous observations concerning inhibitory effects of tGnRH-A on the progestogen and GtH-induced reinitiation of meiosis in the follicle-enclosed goldfish oocytes (H. R. Habibi, G. Van Der Kraak, E. Bulanski, and R. E. Peter, Amer. J. Physiol. 255, R268-R273 (1988] the influence of testosterone on the GtH- and DHP-induced meiosis in vitro was also studied. Testosterone (1 micrograms/ml) enhanced both GtH- and DHP-induced oocyte meiosis in the goldfish oocytes. Testosterone alone was also found to significantly increase oocyte meiosis in the goldfish oocytes in a dose-related fashion. The present findings demonstrate an inhibitory effect of a GnRH agonist on GtH-induced testosterone production in goldfish oocytes and suggest that tGnRH-A might influence oocyte meiosis in part by influencing steroidogenesis.

Animals↗

Evidence for the involvement of endogenous opioids in the regulation of gonadotropin secretion in male goldfish, Carassius auratus.

The in vivo effects of the opioid receptor antagonist naloxone (NAL) alone, and in combination with des-Gly10[D-Ala6]LHRH ethylamide (LHRH-A) and the dopamine receptor antagonist domperidone (DOM) on serum gonadotropic hormone (GtH) levels in male goldfish, Carassius auratus, were investigated. NAL caused a significant decrease in serum GtH 1 hr following treatment, with a return to control levels by 2 hr. NAL treatment attenuated the stimulation of GtH levels in response to DOM; NAL treatment 2 hr prior to or 2 hr following DOM resulted in a significantly reduced response to DOM. During late recrudescence, NAL pretreatment significantly blocked the stimulatory effects of LHRH-A on serum GtH. During early recrudescence, when LHRH-A alone did not significantly elevate GtH levels, NAL treatment simultaneously with or 1 hr following LHRH-A significantly elevated serum GtH. In DOM-pretreated fish, combined LHRH-A and NAL treatment resulted in a nine-fold increase in serum GtH compared to DOM alone. These data indicate the ability of NAL to both suppress and increase GtH levels in male goldfish. Interactions between NAL, DOM, and LHRH-A suggest that opioids modulate both dopamine and GnRH secretion, and possibly the pituitary sensitivity to GnRH and dopamine, thus affecting GtH levels.

Animals↗

In vitro binding characteristics of [3H]spiperone to the pituitary of the goldfish (Carassius auratus).

Homogenates of the pituitary of the goldfish (Carassius auratus) were incubated with [3H]spiperone under various experimental paradigms to evaluate the binding characteristics of the goldfish pituitary dopamine receptor. Binding was tissue specific as binding of [3H]spiperone to goldfish pituitary was greater than other tissue types examined, and the magnitude of binding was found to be dependent on pituitary (protein) content; also, specific binding was heat labile. Association was rapid and binding was reversible (dissociable) by addition of excess competing ligand (domperidone, a specific dopamine D2 receptor antagonist); the half-life (t1/2) of dissociation was 9.2 min and the estimated dissociation rate constant (k-1) was 7.56 x 10(-2) min-1); as well, the association rate was temperature dependent. Binding was saturable; saturation analysis using [3H]spiperone indicated a single class of binding sites with an estimated dissociation constant (Kd) and capacity of 7.39 +/- 1.23 x 10(-6) M and 31.56 +/- 2.72 x 10(-9) mol/mg protein, respectively. [3H]Spiperone binding was displaceable; displacement analysis using unlabeled domperidone indicated a single class of binding sites with estimated Kd and capacity of 2.94 +/- 0.54 x 10(-6) M and 19.47 +/- 3.12 x 10(-9) mol/mg protein, respectively. Binding was specifically inhibited by various dopamine antagonists and agonists. The density of binding sites differed significantly between regions of the goldfish pituitary; the number of binding sites in the pars distalis and neurointermediate lobes was estimated as 38.89 +/- 2.07 x 10(-9) mol/mg protein vs 109.45 +/- 25.33 x 10(-9) mol/mg protein, respectively; while the Kd's estimated as 3.73 +/- 0.248 x 10(-6) M vs 4.1 +/- 1.21 x 10(-6) M, respectively, were not significantly different. These data agree with previous in vivo and in vitro findings of the biological actions of dopamine agonists and antagonists in modifying gonadotropic hormone release in the goldfish and represent the first demonstration of the existence and binding characteristics of a dopamine/neuroleptic receptor in the pituitary of a nonmammalian vertebrate.

Animals↗

Relationship between serum growth hormone levels and the brain and pituitary content of immunoreactive somatostatin in the goldfish, Carassius auratus L.

In this study, the relationships between endogenous brain and pituitary immunoreactive somatostatin (irSRIF) and circulating growth hormone (GH) levels in the goldfish were examined using two approaches. First, the amount of irSRIF in extracts of the pituitary gland and various brain regions was measured by radioimmunoassay several times throughout the year and was compared to serum GH levels at each time. The amounts of irSRIF in extracts of the pituitary gland, hypothalamus, and telencephalon were found to be inversely related to seasonal changes in serum GH levels, such that irSRIF was highest in these regions when serum GH levels were lowest (November and February). Conversely, irSRIF in these regions was lower in May, June, and July when serum GH levels were highest. These results suggest that endogenous irSRIF in the pituitary and forebrain may participate in the regulation of seasonal changes in serum GH levels in the goldfish. In extracts from other brain regions (thalamus + midbrain and cerebellum + medulla), some changes in the amount of irSRIF were observed among the various sample times, but these variations were not related to changes in serum GH levels. In a second set of experiments, the origin of irSRIF fibers innervating the goldfish pituitary gland was examined by using brain lesioning techniques to destroy regions of the forebrain known to contain irSRIF perikarya and fibers, and subsequently measuring the amount of irSRIF in the pituitary gland. Lesions in the preoptic area of the forebrain resulted in increased serum GH levels concomitant with a decrease in pituitary irSRIF content. This provides direct evidence that the preoptic area is the origin of a somatostatinergic projection inhibiting GH secretion from the goldfish pituitary. Lesions centered in the nucleus lateral tuberis (NLT) pars anterioris did not influence serum GH levels or the pituitary content of irSRIF. In contrast, more posterior lesions centered in the NLT pars posterioris (NLTp) resulted in a dramatic reduction in the amount of irSRIF in the pituitary. This suggests that the majority of irSRIF projections to the goldfish pituitary pass through the area destroyed by the lesion centered in the NLTp; it is also possible that perikarya within this area may be the origin of at least some of the irSRIF-containing fibers in the goldfish pituitary. Together, results from the present study provide evidence of a functional relationship between circulating levels of GH and endogenous brain and pituitary irSRIF in the goldfish.

Animals↗

Alterations in pituitary GnRH and dopamine receptors associated with the seasonal variation and regulation of gonadotropin release in the goldfish (Carassius auratus).

Seasonal variations in the serum concentrations of gonadotropin (GtH) and the serum GtH response to intraperitoneal injection of domperidone, a specific dopamine receptor antagonist, were examined in goldfish. In addition, the effects of in vivo treatment of goldfish with a superactive analog of salmon gonadotropin-releasing hormone (sGnRH-A) and domperidone on the binding parameters of pituitary GnRH and dopamine receptors were investigated in goldfish. Serum concentrations of GtH and the maximum GtH response to domperidone increased in correlation with advancing gonadal maturation; values increased from those in sexually regressed fish in January to maximal levels observed in fish in late stages of gonadal recrudescence in March, followed by a decrease with gonadal regression. At all stages, injection of domperidone increased serum concentrations of GtH in a dose-related manner; however, the ED50 of domperidone did not vary significantly over the course of the reproductive cycle. Multiple injections of sGnRH-A caused a progressively increasing and more prolonged serum GtH response; as well, multiple sGnRH-A treatment significantly potentiated the serum GtH response to domperidone without altering the ED50 of domperidone. sGnRH-A treatment caused a significant increase in the number of dopamine/neuroleptic receptors in the goldfish pars distalis, accompanied by a nonsignificant increase in dopamine/neuroleptic receptors in the neurointermediate lobe, and significantly increased the number of high-affinity GnRH receptors in the goldfish pituitary. Treatment with domperidone also significantly increased pituitary high-affinity GnRH receptor numbers. Receptor affinities were not significantly altered by either sGnRH-A or domperidone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Dopamine inhibition of gonadotropin and alpha-melanocyte-stimulating hormone release in vitro from the pituitary of the goldfish (Carassius auratus).

The purpose of the present investigation was to examine the receptor specificity of dopamine inhibition of gonadotropin (GtH) and alpha-melanocyte-stimulating hormone (alpha-MSH) release from the goldfish (Carassius auratus) pituitary in vitro. Pars distalis (PD) and neurointermediate lobe (NIL) fragments of the goldfish pituitary were superfused in vitro under various experimental paradigms; eluate from PD and NIL fragments was analyzed for (GtH) and (alpha-MSH), respectively. Spontaneous GtH release from PD fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited spontaneous GtH release with an estimated ED50 of 10(-4.4) M. Domperidone, a specific D-2 receptor antagonist, reversed the inhibitory action of dopamine and increased spontaneous GtH release. Acute treatment of PD fragments with salmon GnRH (sGnRH) stimulated GtH release; dopamine inhibited GtH release from similarly treated fragments with an ED50 of 10(-7.5) M. The spontaneous release of alpha-MSH from NIL fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited this release with an ED50 of 10(-7.2) M. Acute treatment of NIL fragments with thyrotropin-releasing hormone (TRH) caused acute dose-related increases in alpha-MSH release with an ED50 of 10(-8.2) M; dopamine reversibly inhibited alpha-MSH release from similarly treated fragments with an ED50 of 10(-7.7) M. Both stereoisomers of apomorphine, a dopamine agonist, inhibited GtH release from PD fragments treated with sGnRH; in contrast, alpha-MSH release from NIL fragments treated with TRH was stereospecifically inhibited by (-)-apomorphine, but not by (+)-apomorphine. Domperidone reversed (ED50 = 10(-6.6) M) dopamine (10(-6.3) M) inhibition of GtH release from PD fragments treated with sGnRH. In NIL fragments, the inhibitory action of dopamine (10(-6.3) M) was reversed by domperidone (ED50 = 10(-5.5) M), which restored the acute alpha-MSH release response to TRH. These results suggest the involvement of a low-affinity dopamine/neuroleptic receptor in dopamine inhibition of GtH and alpha-MSH release from the pituitary of the goldfish.

Animals↗

Functional relationship between receptor binding and biological activity for analogs of mammalian and salmon gonadotropin-releasing hormones in the pituitary of goldfish (Carassius auratus).

The relationship between gonadotropin-releasing hormone (GnRH) receptor binding and biological activity in the goldfish pituitary for mammalian and salmon GnRH (sGnRH) analogs with structural modification at the C terminus involving replacement of glycine amide with an alkyl amine and replacement of the Gly6 residue with D amino acids was examined. The GnRH receptor binding data were analyzed with a computerized curve-fitting program (LIGAND) for a single as well as two classes of binding sites; analysis based on one site fit estimated binding affinity and capacity for one class of binding site, and analysis based on two-site fit estimated binding affinity and capacity for two classes of binding sites (high-affinity/low-capacity and low-affinity/high-capacity binding sites). The estimated receptor affinity values were then used to determine the correlation between binding affinity and gonadotropin (GTH)-release potency in vitro. The highest correlation between biological activity and receptor binding affinity was obtained for the high-affinity/low-capacity binding sites and GnRH analogs containing Trp7 and Leu8 residues (i.e., the salmon GnRH structural format) (R = 0.940 +/- 0.150). For the same group of GnRH analogs, there was no significant correlation between the relative GTH-release potency and binding affinity of the low-affinity/high-capacity sites (R = 0.159 +/- 0.434), or that obtained from a one-site fit (R = 0.198 +/- 0.431). Similarly, for mammalian GnRH analogs, significant correlation between binding affinity and biological activity (R = 0.406 +/- 0.049) was only obtained for the high-affinity sites, although the degree of correlation was significantly lower than that obtained for salmon GnRH analogs. The present findings provide strong support for the hypothesis that high-affinity GnRH receptors are involved in the control of GTH release in the goldfish pituitary. In addition, the results demonstrate clearly that the presence of Trp7, Leu8 residues in salmon GnRH molecule, a native peptide in goldfish, is important for recognition of the ligand by the GnRH receptors in the goldfish pituitary, and that structural modifications at positions 6 and 10 in this peptide can increase receptor binding affinity and biological activity at the pituitary level. The most active sGnRH analog identified to date is [D-Arg6, Pro9-NEt]-sGnRH.

Animals↗

Evidence that gonadotropin-releasing hormone also functions as a growth hormone-releasing factor in the goldfish.

The present study examined the influence of GnRH on the in vivo and in vitro secretion of GH in the goldfish (Carassius auratus). Intraperitoneal injection of several GnRH peptides, including a form native to goldfish, salmon GnRH (sGnRH), elevated circulating GH levels in female goldfish. An analog of mammalian GnRH (mGnRH), [D-Ala6,Pro9-NEt] mGnRH (mGnRH-A), at a dosage of 0.1 microgram/g BW increased serum GH levels for up to 48 h after a single ip injection. Goldfish receiving a series of injections of this dose of mGnRH-A also displayed an increased rate of body growth, indicating that the mGnRH-A-induced increase in the circulating GH level was sufficient to accelerate body growth. In vitro experiments using perifused pituitary fragments found that sGnRH stimulated the secretion of GH from the goldfish pituitary in a potent, dose-dependent, and reversible manner. The time course of response and half-maximally effective dose of sGnRH were very similar for both GH and gonadotropin (GTH) secretion in vitro, suggesting that the mechanism(s) mediating the stimulatory actions of GnRH in the goldfish may be similar for both GH and GTH secretion. However, GnRH-induced GH and GTH secretion from the goldfish pituitary can occur independently of each other, as demonstrated by the finding that somatostatin inhibited the GnRH stimulation of GH secretion in vitro, without influencing the GTH response, whereas the dopamine agonist apomorphine inhibited GnRH-induced GTH secretion in vitro, without influencing the GH response. Furthermore, the dopamine antagonist pimozide did not influence serum GH levels, although pimozide potentiated the stimulatory effect of GnRH on GTH secretion in vivo by blocking the endogenous GTH release inhibitory action of dopamine. Results of the present study suggest that the secretion of GH and GTH in the goldfish are regulated, at least in part, through a common releasing factor, GnRH, whereas somatostatin and dopamine appear to act independently as GH and GTH release inhibitory factors, respectively.

Analysis of Variance↗

Dopaminergic regulation of pituitary gonadotrophin-releasing hormone receptor activity in the goldfish (Carassius auratus).

In goldfish, dopamine acts as an endogenous inhibitor of basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release. The purpose of the present study was to investigate the effects of dopamine on the pituitary GnRH receptors in vivo and in vitro in goldfish. The goldfish pituitary contains two classes of GnRH-binding sites, a high-affinity/low-capacity site and low-affinity/high-capacity site. Injection of domperidone, a dopamine antagonist, resulted in a dose- and time-related increase in capacity of both the high- and low-affinity GnRH-binding sites; apomorphine, a dopamine agonist, completely reversed this effect. The effects on GnRH receptor capacity correlated very closely with changes in serum gonadotrophin concentrations. Domperidone was generally without effect on GnRH-binding affinity; however, a small but significant decrease in affinity was observed for the low-affinity binding site at 18 h after injection of the highest dose of domperidone used (40 mumol/kg body weight). Treatment with apomorphine of goldfish pituitary fragments in a perifusion system caused a decrease in the capacity of both the high- and low-affinity GnRH-binding sites without affecting binding affinity; domperidone reversed this effect. It is concluded that the dopaminergic inhibition of basal and GnRH-stimulated gonadotrophin release in goldfish might, in part, be the result of a down-regulation of the pituitary GnRH receptors; this effect of dopamine can be achieved by a direct action at the pituitary level.

Animals↗

Gonadotropin content of the pituitary gland of gonadal tumor-bearing common carp x goldfish hybrids from the Great Lakes, as assessed by bioassay and radioimmunoassay.

The hybrids of carp (Cyprinus carpio) and goldfish (Carassius auratus) collected from the lower Great Lakes between 1978 and 1981 exhibited epizootics of gonadal neoplasm which were rare in the parental species. The pituitary glands of hybrids were, on average, 2.5 times larger than that of carp of similar body size. Histologically, the hypertrophy was due to hyperplasia of proximal pars distalis basophils (the presumptive gonadotropes). Using a carp gonadotropin (GtH) radioimmunoassay it was found that hybrid pituitaries contained more GtH than sympatric carp and that pituitary GtH concentration in hybrids was positively correlated with pituitary weight. Both this and histological evidence suggested that gonadotrope hyperplasia was a progressive event. Two heterologous gonad bioassays indicated that hybrid GtH had biological activity. Whether pituitary hyperplasia in hybrids is a primary problem or secondary to gonadal sterility has not been determined.

Animals↗

Evidence for a gonadotropin-releasing hormone binding protein in goldfish (Carassius auratus) serum.

The binding of salmon gonadotropin-releasing hormone (sGnRH) and its superactive analog, [D-Arg6, Pro9-NEt]-sGnRH, to a macromolecular component in goldfish serum was studied, using 125I-[D-Arg6, Pro9-NEt]-sGnRH and 125I-sGnRH as labeled ligands. Bound was separated from free labeled ligand by gel filtration with Sephadex G-50. The binding of labeled ligand to goldfish serum was dose-dependent. The results indicate a single class of binding site having low affinity and high capacity. The existence of a GnRH binding protein in serum may, in part, contribute to the long-lasting pharmacological action of GnRHs in goldfish.

Animals↗

Effects 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 or domperidone, on gonadotropin release and ovulation in the Chinese loach and common carp.

The effects of LHRH-A and sGnRH-A alone and in combination with the dopamine receptor antagonists pimozide (PIM) and domperidone (DOM) on stimulation of gonadotropin (GtH) secretion and ovulation in Chinese loach (Paramisgurnus dabryanus) and common carp (Cyprinus carpio) were studied. When tested in the absence of a dopamine receptor antagonist, sGnRH-A was about 10-fold more potent than LHRH-A in stimulating GtH secretion in loach, whereas these peptides were of similar effectiveness in common carp. Both peptides were effective alone in inducing ovulation in loach, but were ineffective in common carp. PIM and DOM stimulate a small but significant increase in serum GtH, and greatly potentiate the effects of LHRH-A and sGnRH-A on GtH secretion and ovulation in both species. DOM was of equal or somewhat greater potency than PIM in potentiating the action of releasing hormone agonists in loach; however, DOM had markedly greater effectiveness in common carp. sGnRH-A in the presence of DOM was more effective than LHRH-A in stimulating GtH secretion and ovulation in common carp. The present studies suggest that there are marked differences in the relative contribution of GnRH and dopamine in the control of GtH secretion in loach and common carp, and indicate in particular that the more intense dopaminergic inhibitory control of GtH release in common carp modifies the responsiveness of the pituitary to GnRH peptides.

Animals↗

Isolation and characterization of carp prolactin.

Prolactin (PRL) was extracted with acid-acetone from common carp (Cyprinus carpio) pituitary glands and purified by gel filtration on Sephadex G-75, ion-exchange chromatography on DEAE-cellulose, and reversed-phase high-performance liquid chromatography (HPLC) on TSK-gel TMS 250 with a yield of 0.7 mg/g wet tissue. At each stage of purification, fractions were monitored by HPLC on TSK-gel ODS 120T and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Carp PRL was almost equipotent with ovine PRL in retaining plasma Na concentrations in the hypophysectomized killifish, Fundulus heteroclitus. Immunocytochemistry at both the light and electron microscopic levels revealed that carp PRL antiserum specifically stained cells in the goldfish rostral pars distalis. No cross reaction with putative growth hormone (GH) cells in the proximal pars distalis was observed. The specificity of the carp PRL antiserum was confirmed by immunoblot studies. Although immunostaining of both carp and salmon PRL was observed, there was no cross reaction to GHs from these species. Carp PRL had a sole N-terminal residue of valine, a molecular weight of 23 kDa in SDS-PAGE, and an isoelectric point of 7.3 by gel electrofocusing. Based on these results, together with the knowledge of physicochemical properties of salmon and tilapia PRLs, we propose a standard procedure for isolation of fish PRLs.

Animals↗

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 micrograms/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. Administration 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 micrograms/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 micrograms/g; ip), a 5-HT reuptake inhibitor, potentiated the stimulatory effects of 5-HT on GtH secretion. Ketanserin (10 micrograms/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.

Animals↗

The effects of reserpine and LHRH or salmon GnRH analogues on gonadotropin release, ovulation and spermiation in common carp (Cyprinus carpio L.).

The effects of reserpine (catecholamine depletor) and LHRH analogues on gonadotropin secretion, spermiation and ovulation of common carp were investigated. Injections of reserpine alone at a dose of 1 or 7 mg/kg of body weight stimulated spermiation, and reserpine at a dose of 1 mg/kg of body weight in combination with (D-Arg6, Trp7, Leu8, Pro9, NEt)-LHRH (s-GnRH-A) or with (D-Ala6, Pro9)-LHRH (LHRH-A) at a dose of 50 micrograms/kg of body weight caused an increase of plasma gonadotropin levels, spermiation and ovulation in 80-90% of the females. Simultaneous injection of reserpine and LHRH analogues was as effective as injection of reserpine followed by injection of LHRH analogues 6 h later.

Animals↗