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Biomedical subjects

R E Peter

Publications and source records attributed to R E Peter.

At least 163 records · Page 9Linked to original sources

Structure-activity relationships of mammalian, chicken, and salmon gonadotropin releasing hormones in vivo in goldfish.

Mammalian, chicken, and salmon gonadotropin releasing hormones (GnRHs), and anlogs of each peptide, were injected either alone or in combination with pimozide into goldfish, and the changes in serum gonadotropin (GtH) levels determined. The native peptides had similar potencies in terms of magnitude and duration of the GtH response. Analogs of LHRH that are superactive in mammals are also superactive in goldfish; although [(imBzl)-D-His6, Pro9-NEt]-LHRH is very highly superactive in mammals it has activity similar to [D-Ala6, Pro9-NEt]-LHRH in goldfish. D-Ala6 or (imBzl)-D-His6 substitutions of [Trp7, Leu8, Pro9-NEt]-LHRH are not superactive in goldfish, whereas the D-Arg6 substitution is highly superactive, indicating that there are differences in the factors that make salmon and mammalian GnRH superactive. These results also indicate that the structural modifications that determine superactivity of GnRHs in goldfish differ from what is known for mammals.

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Influences of catecholamines on growth hormone release in female goldfish, Carassius auratus.

The influence of catecholamines on growth hormone (GH) release in female goldfish was investigated by monitoring serum GH levels following injections of drugs known to alter catecholamine synthesis and neural activities. Intraperitoneal (i.p.) injection of 6-hydroxydopamine, a catecholaminergic neurotoxin, or alpha-methyl-p-tyrosine, a catecholamine synthesis inhibitor, decreased serum GH levels. Intraperitoneal injection of L-beta-dihydroxyphenylalanine (L-dopa) increased serum GH concentrations in a dose-dependent manner. The L-dopa-induced increase in serum GH was potentiated by i.p. injection of carbidopa, which would increase the availability of L-dopa to brain tissues by blocking the peripheral conversion of L-dopa to dopamine (DA). These results suggest that L-dopa or one of its catecholamine metabolites acts centrally to increase GH release. Intraventricular (i.v.t.) injection of DA and i.p. injection of apomorphine, a DA agonist that crosses the blood-brain barrier, increased serum GH. Intraperitoneal injection of DA did not alter circulating GH levels in normal fish or fish bearing preoptic lesions that abolish an inhibitory hypothalamic influence on GH release; however, DA increased serum GH in fish which had their blood-brain barrier destroyed by sham operation procedures. These results indicate that DA acts centrally to stimulate GH secretion, possibly by inhibiting the release and/or synthesis of GH release-inhibitory factor. Serum GH concentrations were decreased in a dose-dependent manner by i.p. injection of norepinephrine (NE), whereas i.v.t. injection of NE did not alter serum GH levels. These results indicate that NE acts outside of the blood-brain barrier to decrease serum GH levels in the goldfish, possibly by directly influencing pituitary GH cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Response of superfused goldfish pituitary fragments to mammalian and salmon gonadotropin-releasing hormones.

Salmon and mammalian gonadotropin-releasing hormones (sGnRH, mGnRH) were tested for their ability to stimulate in vitro gonadotropin (GtH) release from superfused goldfish pituitary fragments. A two minute exposure to either peptide was sufficient to stimulate a dose-dependent increase in GtH release which reached maximum levels in 15 minutes and returned to baseline within one hour. Both peptides were approximately equipotent in stimulating GtH release, as was a superactive analog of mGnRH. These results demonstrate that sGnRH is capable of directly stimulating GtH release from teleost pituitary tissue, and that structural differences between the three peptides tested do not result in significant differences in in vitro bioactivity.

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Effects of dopamine and norepinephrine on in vitro spontaneous and gonadotropin-releasing hormone-induced gonadotropin release by dispersed cells or fragments of the goldfish pituitary.

Enzymatically dispersed goldfish pituitary cells or freshly prepared goldfish pituitary fragments continue to secrete gonadotropin spontaneously in a column perifusion system. After the establishment of basal secretion rates, treatment of dispersed pituitary cells with 5 and 500 nM dopamine, or pituitary fragments with 50 and 100 nM dopamine, decreased the amount of gonadotropin released into the perifusate. Perifusion with 500 nM dopamine also abolished the gonadotropin-release response to a 10 nM solution of a luteinizing hormone-releasing hormone analogue in both perifusion systems. Perifusion of pituitary dispersed cells or fragment preparations obtained from sexually regressed goldfish with 50 nM norepinephrine consistently increased the amount of gonadotropin released into the perifusate. These results provide in vitro evidence for direct dopamine inhibition of spontaneous gonadotropin release, blockade by dopamine of gonadotropin-releasing hormone actions, and norepinephrine stimulation of gonadotropin secretion in goldfish.

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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.

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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.

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Effects of catecholaminergic agonists and antagonists on serum gonadotropin concentrations and ovulation in goldfish: evidence for specificity of dopamine inhibition of gonadotropin secretion.

The elevated serum gonadotropin (GtH) levels in goldfish receiving two injections of des Gly10, [D-Ala6] LH-RH ethylamide (LH-RH-A), given 12-hr apart, were reduced by apomorphine, a dopamine agonist, injected at either the first or the second LH-RH-A injection. Serum GtH concentrations in goldfish given two injections of LH-RH-A at a 3-hr interval were also depressed by bromocriptine, a specific D-2 dopamine receptor agonist, administered simultaneously with both LH-RH-A injections. Injections of dopamine antagonists, pimozide or metoclopramide (a specific D-2 antagonist) caused increased serum GtH concentrations in normal goldfish, but no changes were found following injections of the alpha-adrenergic antagonist phentolamine, the beta-adrenergic antagonist propranolol, or the sympathomimetic agent octopamine. Injection of pimozide or metoclopramide at the time of the second of two LH-RH-A injections given at an interval of 12 hr potentiated the LH-RH-A-induced increase in serum GtH concentrations; injections of phentolamine, propranolol, or octopamine did not alter the response to LH-RH-A. Injections of pimozide or metoclopramide also increased the frequency of ovulation in LH-RH-A-injected gravid female goldfish. These results suggest that stimulation of dopamine receptors can block the potentiating effect of multiple injections of GtH-releasing hormone, as well as ongoing LH-RH-A-stimulated release. The results also indicate that the dopamine inhibition of GtH secretion is specific and may be mediated by receptors resembling the D-2 type receptors in mammals.

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Endocrine changes during natural spawning in the white sucker, Catostomus commersoni. I. Gonadotropin, growth hormone, and thyroid hormones.

White suckers (Catostomus commersoni; Cypriniformes, Teleosteii) spawning in a small stream in central Alberta were captured during different stages of their spawning migrations in 1981 and 1982, blood was sampled, and the fish were examined to determine their reproductive condition. Blood samples were analyzed for gonadotropin (GtH), growth hormone (GH), triiodothyronine (T3), and thyroxine (T4) by radioimmunoassay. GtH levels in both sexes were lowest prior to the onset of spawning, increased significantly in spawning males, females in which germinal vesicle migration had begun, and ovulated females and then dropped significantly in spent fish of both sexes. GH was lowest in prespawning females, increased significantly at ovulation, and remained high in spent females. In contrast, GH levels in males were relatively constant throughout spawning. In both sexes, highest T4 levels were found in prespawning fish, and T4 decreased significantly in spent fish. Although a similar decline was seen in T3 in 1981, in 1982 there were no T3 changes associated with changes in reproductive condition. No significant diurnal variations were detected in the levels of GtH or T3; T4 levels appeared to vary on a diurnal basis in prespawning males only. Spawning activity in both sexes therefore appears to be associated with increases in GtH occurring at ovulation in females and at the initiation of spawning in males. GH levels may also be related to reproductive condition in females, but not in males. The relationship of thyroid hormone levels to reproductive condition is less clear, however, and these levels may reflect both endocrine and environmental influences on thyroid function.

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Influences of norepinephrine and alpha-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 (alpha-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 (alpha-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 alpha-adrenergic mechanisms at the brain and/or pituitary level in female goldfish in a sexually regressed or early ovarian recrudescence condition.

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The effects of somatostatin on serum growth hormone levels in the goldfish, Carassius auratus.

In the present study the effects of somatostatin on serum growth hormone (GH) levels in the goldfish, Carassius auratus, were investigated. A single intraperitoneal injection of either 0.1 or 1.0 micrograms somatostatin/g body wt caused a significant decrease in serum GH levels at 1 h postinjection compared to vehicle-injected controls. Two intraperitoneal injections of somatostatin (1.0 micrograms/g body wt), given 12 hr apart, caused a significant decrease in serum GH levels, compared to both presample and vehicle-injected control groups at 1.5 and 6 hr following the second injection. In fish given two injections of somatostatin, a post inhibitory rebound in serum GH levels occurred by 24 hr following the second injection. Thyrotropin-releasing hormone (1 micrograms/g body wt), given as a control peptide, caused a significant increase in serum GH levels at 24 hr, but no significant changes were found at 1.5 or 6 hr following the second of two intraperitoneal injections given 12 hr apart. The increases in serum GH at 24 hr may be due to stress. The results demonstrate that somatostatin causes a transient decrease in blood GH levels in goldfish.

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[Potentiation by pimozide of the effects of LHRH-A on hypophyseal gonadotropin secretion, ovulation and spermiation in the common carp (Cyprinus carpio)].

During the reproductive season in August, we administered to adult male and female Carp an LHRH analog (LHRH-A = D-trp6EA-LHRH) (50 micrograms/kg) alone or in association with pimozide, a dopamine inhibitor (10 mg/kg). LHRH-A caused the circulating portal level of gonadotropin to rise significantly in males and less in females. Spermiation was stimulated in the males and oocyte maturation in females but there was no ovulation. An infection of pimozide and then of LHRH-A 6 h later significantly increased c-GTH secretion and spermiation more than LHRH-A given alone, and induced ovulation in the females.

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Entrainment of daily serum gonadotropin cycles in the goldfish to photoperiod, feeding, and daily thermocycles.

Female fish were kept under 16L:8D/20 degrees C in November and April and the onset of light and/or feeding times were shifted by several hours in the experimental groups. Photoperiod and feeding entrained significant fluctuations in serum gonadotropin hormone (GTH) levels when the onset of light and the first daily feeding were 4 hr apart, but not when they were 10 hr apart. Fish were subjected to 16L:8D for 14-16 days in February, and to either a constant warm (20 degrees C) or a diurnal sinusoidal (12-20 degrees C) temperature regime, the warmth being imposed during photophase or scotophase. While relatively high, uniform serum GTH levels were found throughout the 24-hr period in fish subjected to constant warmth, warm temperature during the day promoted fluctuations in serum GTH levels, and warmth during night resulted in relatively low, uniform serum GTH levels.

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Characteristics and functional significance of daily cycles in serum gonadotropin hormone levels in the goldfish.

Goldfish were subjected to 12L:12D/12 degrees C, 16L:8D/20 degrees C, or to an outdoor pond regime for various lengths of time at several times of year. Serum gonadotropin hormone (GTH) levels were determined through 24-h periods and ovaries were examined histologically. Low and uniform serum GTH levels were found throughout the day in fish under 12L:12D/12 degrees C for 32 days in November; significant fluctuations were found under this regime after 32 days in March. In fish held under 16L:8D/20 degrees C, a peak in serum GTH levels was detected after 7 days in November and after 13 days in March. GTH levels were high and uniform throughout the day after 32 days in November and March. Patterns of daily cycles in serum GTH levels of fish kept in an outdoor pond were similar to the patterns detected in the laboratory under similar conditions of photoperiod and temperature. Fluctuating serum GTH levels were correlated with greater oocyte growth than constant low levels. Constant high serum GTH levels were correlated with oocyte atresia.

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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 alpha-methyl-para-tyrosine and carbidopa, respectively, but not norepinephrine by diethyldithiocarbamate, raised serum GtH values above those of controls. Injections of an alpha-agonist, clonidine, also increased serum GtH concentrations. These results suggest the existence of an inhibitory dopaminergic and a stimulatory alpha-adrenergic influence on GtH release in goldfish.

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Effects of monosodium L-glutamate on pituitary innervation in goldfish, Carassius auratus.

Monosodium L-glutamate was injected intraperitoneally into goldfish at a dosage of 2.5 mg/g body wt. The first noticeable effect in the pituitary, 30 min postinjection, was marked swelling of pituicytes in the neurohypophysis (NH). Eighteen hours postinjection a large number of degenerating type B fibers were found in the NH of the proximal pars distalis (PPD), while all type A fibers, and type B fibers in other parts of the pituitary, remained unaffected. Because glutamate causes a lesion in the nucleus lateral tuberis (NLT), from the anterior margin of the pituitary stalk through to the posterior end of the nucleus, and a minor lesion in the nucleus preopticus periventricularis, it is likely that the NLT is the origin of the degenerative type B fibers in the proximal NH. The significance of these results is discussed in relation to the neuroendocrine regulation of the pituitary functions in goldfish.

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Effects of hypothalamic lesions on serum growth hormone levels and growth rates in goldfish, Carassius auratus.

Serum growth hormone (GH) levels and growth rates of goldfish were measured concurrently following discrete electrothermic lesions of a number of hypothalamic nuclei. Following lesions of the nucleus preopticus periventricularis (NPP), significant increases in serum GH levels were evident at 4 weeks postlesioning in comparison to both sham-operated and normal control groups. In addition, the NPP-lesioned fish showed significant increases in both total body weight and standard length increments compared to control groups. Lesions in other hypothalamic areas including the nucleus anterior tuberis, nucleus lateralis tuberis and the nucleus recessus lateralis had no consistent effect on growth rates or serum GH levels. The present results suggest that the NPP is concerned with the inhibition of GH secretory function in the goldfish.

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Effects of pimozide and des Gly10,[D-Ala6]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 degrees, a single injection of des Gly10,[D-Ala6]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.

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