Selective depletion of dopamine in the goldfish pituitary caused by domperidone

1991 ◽  
Vol 69 (6) ◽  
pp. 776-781 ◽  
Author(s):  
B. D. Sloley ◽  
V. L. Trudeau ◽  
J. G. Dulka ◽  
R. E. Peter
Keyword(s):  
Sch 23390 ◽  
Female Fish ◽  
Antagonist Activity ◽  
Male And Female ◽  
Selective Depletion ◽  
Serum Gonadotropin ◽  
Mouse Pituitary ◽  
Dose Dependent

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, α-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.Key words: domperidone, dopamine, noradrenaline, 5-hydroxytryptamine, pituitary, hypothalamus, telencephalon, gonadotropin, goldfish.

The Display Behavior of Bavia-Aericeps (Araneae, Salticidae), a Jumping Spider From Queensland

1986 ◽  
Vol 34 (3) ◽  
pp. 381 ◽  
Author(s):  
RR Jackson
Keyword(s):  
Adult Female ◽  
Minor Importance ◽  
Mating Tactics ◽  
Jumping Spider ◽  
Male And Female ◽  
Display Behavior ◽  
Location Type

Bavia aericeps Simon is a large plurident jumping spider that frequents palms and other trees in tropical Queensland, building unusually strong and spacious nests on the undersides of leaves. The display repertoire of this species is large and complex, numerous distinct visual, vibratory, and tactile signals being used. Courtship is versatile, each male using one of three different mating tactics depending on the female's maturity and location. Type 1 courtship, involving specialized movements and postures of the legs, palps, and body, occurs if the female is an adult away from the nest; apparently this type of courtship is vision- dependent. If the male encounters an adult female inside her nest, he uses Type 2 courtship, which consists of movements that cause the silk to vibrate. If the female is a subadult inside her nest, the male initially uses Type 2 courtship, then builds a second chamber on the female's nest and cohabits until she moults and matures. Other displays occur during male-male and female-female interactions. Male-male interactions are particularly ferocious, the spiders often being upended and stunned. However, cannibalism seems to be of minor importance in this species.

Modulation of adiponectin system expression in the porcine uterus during early pregnancy by prostaglandin E2 and F2α

2017 ◽  
Vol 29 (9) ◽  
pp. 1832 ◽  
Author(s):  
Kamil Dobrzyn ◽  
Nina Smolinska ◽  
Karol Szeszko ◽  
Marta Kiezun ◽  
Anna Maleszka ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Oestrous Cycle ◽  
Receptor Type ◽  
Adiponectin Receptor ◽  
Pcr Method ◽  
Pg E2 ◽  
Dose Dependent

Studies have demonstrated that adiponectin could be a link between reproductive functions and energy metabolism in animals. The aim of the present study was to investigate the effects of prostaglandin (PG) E2 and PGF2α (10, 50, 100, 250 and 500 ng mL–1) on the expression and secretion of adiponectin and its receptor genes and proteins by cultured in vitro porcine endometrial and myometrial tissues on Days 10–28 of pregnancy and Days 10–11 of the oestrous cycle. The gene expression was analysed using the real-time PCR method. Adiponectin protein secretion was determined by ELISA, whereas the receptors proteins content was defined using Western Blot analysis. Both PGE2 and PGF2α modulated the expression of adiponectin system genes and proteins in the uterus during early pregnancy. PGE2 and PGF2α had similar effects on the adiponectin system, which differed between the stages of gestation and between pregnancy and the oestrous cycle. On Days 10–11 of gestation, PGE2 and PGF2α generally increased adiponectin secretion by endometrial and myometrial tissues. Both PGs decreased levels of endometrial adiponectin receptor type 1 (AdipoR1), whereas only PGF2α decreased myometrial levels of AdipoR1. Both PGs increased myometrial adiponectin receptor type 2 (AdipoR2) levels. On Days 12–13 of gestation, PGE2 decreased AdipoR1 concentrations in both tissues and AdipoR2 levels in the endometrium. PGF2α decreased myometrial concentrations of both receptors. On Days 15–16 of gestation, both PGE2 and PGF2α increased concentrations of AdipoR1 and AdipoR2 in the endometrium and myometrium. PGE2 stimulated the secretion of adiponectin in the endometrium, but not in the myometrium. On Days 27–28 of pregnancy, both PGE2 and PGF2α inhibited the expression of AdipoR1 and AdipoR2 in endometrial and myometrial tissues and decreased the secretion of endometrial adiponectin. Both PGE2 and PGF2α had tissue-specific and dose-dependent effects on the adiponectin system.

scholarly journals Lipid Peroxidation and Antioxidant Status in Male and Female Patients with Type 1 and Type 2 Diabetes Mellitus

Med Phoenix ◽  
2017 ◽  
Vol 1 (1) ◽  
pp. 10-14
Author(s):  
Nirjala Laxmi Madhikarmi ◽  
Prem Prakash Singh ◽  
Tarannum Khatun
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Lipid Peroxidation ◽  
Antioxidant Status ◽  
Total Antioxidant Activity ◽  
Male And Female ◽  
Total Antioxidant

Background: Free radicals are reactive oxygen species which cause lipid peroxidation precipitating many metabolic diseases including Diabetes Mellitus. However, these free radicals are quenched by substances known as antioxidants like vitamin C, vitamin E and several other compounds. Lipid peroxidation and antioxidant status were investigated in patients with Type 1 and Type 2 Diabetes mellitus- Pokhara, Nepal.Methods: The extent of lipid peroxidation was assessed by thiobarbituric acid reactive substances and the antioxidant parameter estimations were total antioxidant activity, Vitamin C and Vitamin E assessed in Type 1 and 2 diabetes mellitus patients along with matched healthy counterparts.Results: The lipid peroxidation was increased in male Type 1 and 2 diabetic patients whereas female group showed decreased level as compared to its healthy counterparts. Similarly, the total antioxidant activity was found to be decreased in the diabetic group. The lipid peroxidation parameter and antioxidant status were statistically significant at p< 0.05.Conclusion: Oxidative stress and antioxidant status varied in male and female patients suffering from diabetes either Type 1 or Type 2. Apart from gender basis of evaluating oxidative stress, variables based on diet, habitat, socioeconomic status, education, etc. can also be considered.MED Phoenix Volume (1), Issue (1) July 2016, page: 10-14

Control of fibroblast growth factor receptor kinase signal transduction by heterodimerization of combinatorial splice variants

1993 ◽  
Vol 13 (7) ◽  
pp. 3907-3918
Author(s):  
E Shi ◽  
M Kan ◽  
J Xu ◽  
F Wang ◽  
J Hou ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Splice Variants ◽  
Sh2 Domain ◽  
Scatchard Analysis ◽  
Fibroblast Growth ◽  
Dose Dependent

A differentiated liver cell (HepG2), which exhibits a dose-dependent growth-stimulatory and growth-inhibitory response to heparin-binding fibroblast growth factor type 1 (FGF-1), displays high- and low-affinity receptor phenotypes and expresses specific combinatorial splice variants alpha 1, beta 1, and alpha 2 of the FGF receptor (FGF-R) gene (flg). The extracellular domains of the alpha and beta variants consist of three and two immunoglobulin loops, respectively, while the intracellular variants consist of a tyrosine kinase (type 1) isoform and a kinase-defective (type 2) isoform. The type 2 isoform is also devoid of the two major intracellular tyrosine autophosphorylation sites (Tyr-653 and Tyr-766) in the type 1 kinase. An analysis of ligand affinity, dimerization, autophosphorylation, and interaction with src homology region 2 (SH2) substrates of the recombinant alpha 1, beta 1, and alpha 2 isoforms was carried out to determine whether dimerization of the combinatorial splice variants might explain the dose-dependent opposite mitogenic effects of FGF. Scatchard analysis indicated that the alpha and beta isoforms exhibit low and high affinity for ligand, respectively. The three combinatorial splice variants dimerized in all combinations. FGF enhanced dimerization and kinase activity, as assessed by receptor autophosphorylation. Phosphopeptide analysis revealed that phosphorylation of Tyr-653 was reduced relative to phosphorylation of Tyr-766 in the type 1 kinase component of heterodimers of the type 1 and type 2 isoforms. The SH2 domain substrate, phospholipase C gamma 1 (PLC gamma 1), associated with the phosphorylated type 1-type 2 heterodimers but was phosphorylated only in preparations containing the type 1 kinase homodimer. The results suggest that phosphorylation of Tyr-653 within the kinase catalytic domain, but not Tyr-766 in the COOH-terminal domain, may be stringently dependent on a trans intermolecular mechanism within FGF-R kinase homodimers. Although phosphotyrosine 766 is sufficient for interaction of PLC gamma 1 and other SH2 substrates with the FGF-R kinase, phosphorylation and presumably activation of substrates require the kinase homodimer and phosphorylation of Tyr-653. We propose that complexes of phosphotyrosine 766 kinase monomers and SH2 domain signal transducers may constitute unactivated presignal complexes whose active or inactive fate depends on homodimerization with a kinase or heterodimerization with a kinase-defective monomer, respectively. The results suggest a mechanism for control of signal transduction by different concentrations of ligand through heterodimerization of combinatorial splice variants from the same receptor gene.

Serotonin enhances oestradiol production by hamster preovulatory follicles in vitro: effects of experimentally induced atresia

1990 ◽  
Vol 125 (3) ◽  
pp. 433-438 ◽  
Author(s):  
P. F. Terranova ◽  
J. Th. J. Uilenbroek ◽  
L. Saville ◽  
D. Horst ◽  
Y. Nakamura
Keyword(s):  
Cyclic Amp ◽  
Dependent Manner ◽  
Glucose Medium ◽  
Preovulatory Follicles ◽  
In Vitro Effects ◽  
Dose Dependent ◽  
Oestradiol Production

ABSTRACT Preovulatory follicles from adult hamsters on the morning of pro-oestrus were used in this study. Serotonin stimulated oestradiol production by preovulatory follicles during a 5-h incubation in 1 ml Krebs–Ringer bicarbonate glucose medium containing isobutylmethylxanthine (0.1 mmol/l; IBMX) and androstenedione (1 μmol/l). The enhanced oestradiol production by serotonin was dependent on the dose of IBMX and androstenedione. Mianserin, a serotonin type-1 and serotonin type-2 receptor antagonists, prevented the serotonin-enhanced oestradiol production in a dose-dependent manner. Ketanserin, a specific serotonin type-2 receptor antagonist, was ineffective in blocking the action of serotonin, indicating that the effect of serotonin was mediated by the serotonin type-1 receptor. In the presence of androstenedione (1 μmol/l), serotonin was unable to enhance oestradiol production in isolated granulosa cells. It was also unable to enhance oestradiol production in early atretic follicles; atresia was induced experimentally by an injection of phenobarbital in order to prevent ovulation. The data indicate that serotonin stimulates oestradiol production by hamster preovulatory follicles in vitro. The mechanism of action of serotonin involves an intact healthy follicle, a serotonin type-1 receptor and possibly cyclic AMP. The increased oestradiol secretion might be related to increased androgen production by the follicle and increased permeability (leakiness) of the follicle to androstenedione which serves as substrate for aromatization to oestradiol by the granulosa cell. Journal of Endocrinology (1990) 125, 433–438

scholarly journals Expression of Type 2 Iodothyronine Deiodinase in Corticotropin-Secreting Mouse Pituitary Tumor Cells Is Stimulated by Glucocorticoid and Corticotropin-Releasing Hormone

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4459-4465 ◽  
Author(s):  
Osamu Araki ◽  
Tadashi Morimura ◽  
Takayuki Ogiwara ◽  
Haruo Mizuma ◽  
Masatomo Mori ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Pituitary Tumor ◽  
Northern Analysis ◽  
Dependent Manner ◽  
Iodothyronine Deiodinase ◽  
Mouse Pituitary ◽  
Dose Dependent ◽  
Menten Constant

We identified the presence of iodothyronine deiodinase in AtT-20 mouse pituitary tumor cells that secrete corticotropin. Iodothyronine deiodinating activity in AtT-20 cells fulfills all the characteristics of type 2 iodothyronine deiodinase (D2), including the inhibition by thyroid hormones, the insensitivity to inhibition by 6-propyl-2-thiouracil, and the low Michaelis-Menten constant value for T4. Northern analysis using mouse D2 cRNA probe demonstrated the hybridization signal of approximately 7.0 kb in size in AtT-20 cells. D2 activity and D2 mRNA were stimulated by glucocorticoid in a dose-dependent manner but were not stimulated by testosterone or β-estradiol. D2 expression was stimulated by (Bu)2cAMP, and CRH in a dose-dependent manner in the presence of dexamethasone. These results suggest the previously unrecognized role of local thyroid hormone activation by D2 in the regulation of pituitary corticotrophs.

Differential Regulation of Glucose Transporters Mediated by CRH Receptor Type 1 and Type 2 in Human Placental Trophoblasts

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1464-1471 ◽  
Author(s):  
Lu Gao ◽  
Chunmei Lv ◽  
Chen Xu ◽  
Yuan Li ◽  
Xiaorui Cui ◽  
...  
Keyword(s):  
Normal Development ◽  
Glucose Transporters ◽  
Differential Regulation ◽  
Regulatory Mechanisms ◽  
Dependent Manner ◽  
Glut1 Expression ◽  
Crh Receptor Type 1 ◽  
Dose Dependent

Glucose transport across the placenta is mediated by glucose transporters (GLUT), which is critical for normal development and survival of the fetus. Regulatory mechanisms of GLUT in placenta have not been elucidated. Placental CRH has been implicated to play a key role in the control of fetal growth and development. We hypothesized that CRH, produced locally in placenta, could act to modulate GLUT in placenta. To investigate this, we obtained human placentas from uncomplicated term pregnancies and isolated and cultured trophoblast cells. GLUT1 and GLUT3 expressions in placenta were determined, and effects of CRH on GLUT1 and GLUT3 were examined. GLUT1 and GLUT3 were identified in placental villous syncytiotrophoblasts and the endothelium of vessels. Treatment of cultured placental trophoblasts with CRH resulted in an increase in GLUT1 expression while a decrease in GLUT3 expression in a dose-dependent manner. Cells treated with either CRH antibody or nonselective CRH receptor (CRH-R) antagonist astressin showed a decrease in GLUT1 and an increase in GLUT3 expression. CRH-R1 antagonist antalarmin decreased GLUT1 expression while increased GLUT3 expression. CRH-R2 antagonist astressin2b increased the expression of both GLUT1 and GLUT3. Knockdown of CRH-R1 decreased GLUT1 expression while increased GLUT3 expression. CRH-R2 knockdown caused an increase in both GLUT1 and GLUT3 expression. Our data suggest that, in placenta, CRH produced locally regulates GLUT1 and GLUT3 expression, CRHR1 and CRHR2-mediated differential regulation of GLUT1 and GLUT3 expression. Placental CRH may regulate the growth of fetus and placenta by modulating the expression of GLUT in placenta during pregnancy.

scholarly journals Fate of Deoxynivalenol in Different Corn Cultivars: From Grains to Bread

2021 ◽  
Author(s):  
Shahzad Zafar Iqbal ◽  
Ahmad Faizal Abdull Razis ◽  
Sunusi Usman ◽  
Nada Basheir Ali ◽  
Muhammad Rafique Asi
Keyword(s):  
Hazard Quotient ◽  
Dietary Exposure ◽  
Average Level ◽  
Percentage Reduction ◽  
Male And Female ◽  
Type 3 ◽  
Corn Grain ◽  
Corn Grains

The objectives of the current research were to determine the levels of deoxynivalenol (DON) in four different cultivars of corn and subsequently to investigate the fate of DON during pro-cessing steps involved for the production of cornbread. The samples (n = 30) of each cultivar which were found positive were selected for the study. The average level of DON was ranged from LOD to 650 &micro;g/kg. The amount of DON in cornflour samples were ranged from LOD to 630 &micro;g/kg and insignificantly lower than the levels found in corn grain samples (p &ge; 0.05). Further-more, the levels of DON in corn dough samples were insignificantly higher than the levels in cornflour samples (p &ge; 0.05), with levels ranged from LOD to 645 &micro;g/kg. However, the amount of DON in cornbread samples was significantly different from the levels found in corn grains sam-ples (p &le; 0.05), with levels ranged from LOD to 611.5 &micro;g/kg. The percentage reduction of DON in grains to cornbread samples was 22.4%, 35.6%, 44.5%, and 42.6% in type 1, type 2, type 3, and type 4 cultivars, respectively. The highest dietary exposure and hazard quotient (HQ) of DON was 0.13 and 0.17 &micro;g/kg bw/d, in male and female individuals resulted from the consumption of cornbread samples, respectively.

Role of serotonin type 2 receptors in regulation of aldosterone production

1985 ◽  
Vol 249 (2) ◽  
pp. E234-E238 ◽  
Author(s):  
H. Matsuoka ◽  
M. Ishii ◽  
A. Goto ◽  
T. Sugimoto
Keyword(s):  
Serotonin Antagonists ◽  
Camp Production ◽  
Inhibitory Effects ◽  
Aldosterone Production ◽  
Dose Dependent Fashion ◽  
Dose Dependent

It is well recognized that serotonin stimulates aldosterone production by the adrenal glands. To investigate the possible roles of serotonin type 1 and 2 receptors in the regulation of aldosterone production, we examined the effects of cyproheptadine (a serotonin antagonist that inhibits both type 1 and 2 receptors) and ketanserin (a serotonin type 2 selective antagonist) on aldosterone and cAMP production in collagenase dispersed rat adrenal capsular cells. Serotonin, ranging in concentration from 10(-9) to 10(-3) M, significantly increased aldosterone production in a dose-dependent fashion after 2 h of incubation at 37 degrees C. Cyproheptadine and ketanserin showed comparable inhibitory effects on basal aldosterone production. These serotonin antagonists preferentially inhibited serotonin-induced aldosterone production. Serotonin significantly increased cAMP production at a dose of 10(-6) M. Both cyproheptadine and ketanserin significantly decreased basal cAMP production at doses of 10(-5) M. These serotonin antagonists preferentially inhibited serotonin-stimulated cAMP production. These results suggest that adrenal serotonin type 2 receptors may be coupled with adenylate cyclase activity and that these receptors are involved in the regulation of aldosterone production. Whether serotonin plays an important role in the regulation of aldosterone secretion in vivo remains to be elucidated.

scholarly journals Control of fibroblast growth factor receptor kinase signal transduction by heterodimerization of combinatorial splice variants.

1993 ◽  
Vol 13 (7) ◽  
pp. 3907-3918 ◽  
Author(s):  
E Shi ◽  
M Kan ◽  
J Xu ◽  
F Wang ◽  
J Hou ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Splice Variants ◽  
Sh2 Domain ◽  
Scatchard Analysis ◽  
Fibroblast Growth ◽  
Dose Dependent

A differentiated liver cell (HepG2), which exhibits a dose-dependent growth-stimulatory and growth-inhibitory response to heparin-binding fibroblast growth factor type 1 (FGF-1), displays high- and low-affinity receptor phenotypes and expresses specific combinatorial splice variants alpha 1, beta 1, and alpha 2 of the FGF receptor (FGF-R) gene (flg). The extracellular domains of the alpha and beta variants consist of three and two immunoglobulin loops, respectively, while the intracellular variants consist of a tyrosine kinase (type 1) isoform and a kinase-defective (type 2) isoform. The type 2 isoform is also devoid of the two major intracellular tyrosine autophosphorylation sites (Tyr-653 and Tyr-766) in the type 1 kinase. An analysis of ligand affinity, dimerization, autophosphorylation, and interaction with src homology region 2 (SH2) substrates of the recombinant alpha 1, beta 1, and alpha 2 isoforms was carried out to determine whether dimerization of the combinatorial splice variants might explain the dose-dependent opposite mitogenic effects of FGF. Scatchard analysis indicated that the alpha and beta isoforms exhibit low and high affinity for ligand, respectively. The three combinatorial splice variants dimerized in all combinations. FGF enhanced dimerization and kinase activity, as assessed by receptor autophosphorylation. Phosphopeptide analysis revealed that phosphorylation of Tyr-653 was reduced relative to phosphorylation of Tyr-766 in the type 1 kinase component of heterodimers of the type 1 and type 2 isoforms. The SH2 domain substrate, phospholipase C gamma 1 (PLC gamma 1), associated with the phosphorylated type 1-type 2 heterodimers but was phosphorylated only in preparations containing the type 1 kinase homodimer. The results suggest that phosphorylation of Tyr-653 within the kinase catalytic domain, but not Tyr-766 in the COOH-terminal domain, may be stringently dependent on a trans intermolecular mechanism within FGF-R kinase homodimers. Although phosphotyrosine 766 is sufficient for interaction of PLC gamma 1 and other SH2 substrates with the FGF-R kinase, phosphorylation and presumably activation of substrates require the kinase homodimer and phosphorylation of Tyr-653. We propose that complexes of phosphotyrosine 766 kinase monomers and SH2 domain signal transducers may constitute unactivated presignal complexes whose active or inactive fate depends on homodimerization with a kinase or heterodimerization with a kinase-defective monomer, respectively. The results suggest a mechanism for control of signal transduction by different concentrations of ligand through heterodimerization of combinatorial splice variants from the same receptor gene.

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