scholarly journals GnRH-I and GnRH-II-induced calcium signaling and hormone secretion in neonatal rat gonadotrophs

2009 ◽  
pp. 709-716
Author(s):  
A Balík ◽  
M Jindřichová ◽  
S Bhattacharyya ◽  
H Zemková
Keyword(s):  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Cyclic Nucleotide ◽  
Hormone Secretion ◽  
Calcium Oscillations ◽  
Melatonin Receptors ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Dependent Manner ◽  
Gonadotropin Release

Two forms of gonadotropin-releasing hormone (GnRH), GnRH-I and GnRH-II, are commonly present in mammals. The main hormone controlling reproduction is GnRH-I acting through its receptor (GnRHR-I), whereas the function of GnRH-II is unknown. In primates, it has been suggested that GnRH-II is a specific agonist for the structurally distinct GnRHR-II. Here we compared effects of GnRH-I and GnRH-II on intracellular calcium and gonadotropin hormone release in neonatal rat gonadotrophs in vitro and the dependence of agonist actions on cyclic nucleotide levels. Both agonists elevated intracellular calcium and stimulated gonadotropin secretion in a concentration-dependent manner, with comparable peak amplitudes, but GnRH-I was three times more potent than GnRH-II. Antide, a specific GnRHRI antagonist, completely blocked the action of both agonists on gonadotropin release. Inhibition of adenylyl cyclase activity by melatonin and MDL significantly attenuated GnRH-I- and GnRHII-induced calcium signaling and gonadotropin release, whereas inhibition of soluble guanylyl cyclase activity was ineffective. GnRH-II also generated calcium oscillations in a fraction of gonadotrophs not expressing melatonin receptors. These results indicate that GnRH-I and GnRH-II act on the same GnRHR to stimulate gonadotropin release through intracellular calcium and cyclic nucleotide signaling, and that GnRH-II is less potent agonist for this receptor in neonatal rat gonadotrophs.

scholarly journals cADP-ribose formation by blood platelets is not responsible for intracellular calcium mobilization

1998 ◽  
Vol 331 (2) ◽  
pp. 431-436 ◽  
Author(s):  
Philippe OHLMANN ◽  
Claude LERAY ◽  
Catherine RAVANAT ◽  
Adel HALLIA ◽  
Dominique CASSEL ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Plasma Membranes ◽  
Calcium Release ◽  
Blood Platelets ◽  
Human Platelets ◽  
Cyclase Activity ◽  
Dependent Manner ◽  
Intact Cells ◽  
Adp Ribosyl Cyclase ◽  
Intracellular Calcium Mobilization

Human platelet CD38 is a multifunctional ectoenzyme catalysing the synthesis and hydrolysis of cADP-ribose (cADPR), a recently identified calcium-mobilizing agent that acts independently of d-myo-inositol 1,4,5-trisphosphate and is known to be expressed by human platelets. The present work shows that ADP-ribosyl cyclase activity is exclusively a membrane activity, of which the major part is located in plasma membranes and a small part in internal membranes. In broken cells, cyclase activity was insensitive to the presence of calcium and was not modulated by agonists such as thrombin or ADP, whereas in intact cells thrombin increased cADPR formation by 30%, an effect due to fusion of granules with the plasma membrane. In order to assess the role of cADPR as a calcium-mobilizing agent, vesicles were prepared from internal membranes and loaded with 45CaCl2. These vesicles were efficiently discharged by IP3 in a dose-dependent manner, but were not responsive to cADPR or ryanodine in the presence or absence of calmodulin. Thus cADPR is unlikely to play a role in intracellular calcium release in human blood platelets.

THE ROLE OF INTERNAL NOISE FOR OPTIMAL INTRACELLULAR CALCIUM SIGNALING IN COUPLED BIOLOGICAL CELL SYSTEM

2011 ◽  
Vol 10 (01) ◽  
pp. 31-39 ◽  
Author(s):  
HONGYING LI ◽  
JIANHONG BI
Keyword(s):  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Cell Size ◽  
Internal Noise ◽  
System Size ◽  
Cell System ◽  
Calcium Oscillations ◽  
Biological Cell ◽  
Intracellular Calcium Signaling

We have studied the role of internal noise for intracellular calcium signaling in coupled biological cell system. It is found that internal noise can induce calcium oscillations and the performance of such oscillations shows two peaks with the variation of the cell size-Ω for any cell chain length-N, indicating the occurrence of system size bi-resonance or internal noise stochastic bi-resonance, which may be very relevant to the canard explosion. We also find that there exists an optimal cell chain length-N for the first peak at which the collective calcium oscillations show the best performance, it is also a phenomenon of "system size resonance". It is interesting to note that one of the optimal cell sizes is present at Ω ~ 103μm3, which is close to a real living cell size in vivo.

Lysophosphatidylcholine elicits intracellular calcium signaling in a GPR55-dependent manner

2017 ◽  
Vol 489 (2) ◽  
pp. 242-247 ◽  
Author(s):  
Anna Drzazga ◽  
Agata Sowinska ◽  
Agnieszka Krzeminska ◽  
Przemysław Rytczak ◽  
Maria Koziolkiewicz ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Dependent Manner ◽  
Intracellular Calcium Signaling

The somatotrope: an endocrine cell with functional calcium transients

1988 ◽  
Vol 139 (1) ◽  
pp. 169-179
Author(s):  
M. O. Thorner ◽  
R. W. Holl ◽  
D. A. Leong
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Hormone Secretion ◽  
Extracellular Calcium ◽  
Calcium Oscillations ◽  
Calcium Transients ◽  
Male Rats ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Gh Secretion

Growth hormone (GH) secretion by the somatotrope is under dual regulation by the hypothalamic peptides, somatostatin (SS) and GH-releasing hormone (GHRH). Cytosolic free calcium concentration and cumulative GH release were measured simultaneously in anterior pituitary cells from adult male rats. This was made possible using a combination of digital imaging video microscopy with the fluorescent calcium indicator Fura-2 and the reverse haemolytic plaque assay (RHPA) to identify the cell type and measure hormone secretion from the cells under study. This technique allows calcium measurements to be made at very short time intervals (less than 150 ms) in single cells. Spontaneous calcium transients were demonstrated in 85% of GH plaque-forming cells. These occurred at a frequency of 2–13 min-1 and had an amplitude of 50–500 nmoll-1. The somatotropes with the largest calcium fluctuations produced the largest plaques; thus, the calcium transients appeared to correlate with hormone release. Since the somatotrope alone shows these fluctuations, the mean intracellular calcium concentration is 238 +/− 18 nmoll-1 in somatotropes and 113 +/− 8 nmoll-1 in non-somatotropes. Upon exposure to SS (1 nmoll-1) intracellular calcium fell from 200–250 nmoll-1 to 50–100 nmoll-1 with an apparent reduction in oscillations. Withdrawal of SS increased the intracellular calcium level. GHRH increased intracellular calcium but 10 nmoll-1 GHRH given simultaneously with 1 nmoll-1 SS reduced intracellular calcium to that level observed during SS alone. Thus, the SS effect on intracellular calcium predominates. The effects of SS can be mimicked by removal of extracellular calcium, or by the addition of CoCl2 (2 nmoll-1) or by verapamil (100 mumoll-1), two agents which block calcium channels. The hormone secretion index (indicated by the area of the plaque formed in RHPA) enables us to demonstrate that GHRH in this system increases GH secretion, and SS inhibits it. In combination, GHRH and SS oppose one another. Spontaneous calcium oscillations are characteristic for normal somatotropes. These oscillations are related to spontaneous hormone secretion and due to influx of calcium through ion channels in the membrane. Intracellular signalling information may be encoded in both frequency and amplitude of calcium oscillations. The actions of GHRH and SS on regulation of GH secretion are proposed to be mediated, at least in part, by regulation of intracellular cytosolic free calcium. This modulation is dependent on extracellular calcium concentrations. We are now investigating the molecular mechanisms involved in this process.

The Calcineurin/NFAT Signaling Pathway Is a Target for the Collagen Type I-Induced Calcium Response in Megakaryocytes and Mediates Expression of Megakaryocytic Genes.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3647-3647
Author(s):  
Satu Kyttaelae ◽  
Ivonne Habermann ◽  
Martin Bornhaeuser ◽  
Gerhard Ehninger ◽  
Alexander Kiani
Keyword(s):  
Cyclosporin A ◽  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Signaling Pathway ◽  
Fas Ligand ◽  
Collagen Type ◽  
Type I ◽  
Dependent Manner ◽  
Transcriptional Responses ◽  
Central Function

Abstract Megakaryocytes, as precursor cells of platelets, comprise a cell population crucial for the maintenance of adult hematopoiesis. Since platelets are anuclear cellular fragments, the platelet transcriptome as well as the proteome are largely determined by the megakaryocyte. Calcium signaling in response to agonists such as collagen or thrombin has a central function in platelet activation and therefore likely represents an important signaling pathway in megakaryocytes as well. Indeed, megakaryocytes show considerable elevation of intracellular calcium levels in response to selected platelet agonists, but the downstream effector molecules of calcium signaling in these cells or the transcriptional responses induced are unknown. We here establish calcineurin and the NFAT (Nuclear Factor of Activated T cells) family of transcription factors as components of a calcium-induced signaling cascade in megakaryocytes. In resting megakaryocytes, NFAT is cytoplasmic and inactive, but can be activated by fibrillar collagen type 1, a physiological agonist of platelets and megakaryocytes known to induce a sustained increase in intracellular calcium levels in these cells. In contrast, treatment with SDF-1a, thrombopoietin, or VEGF remained without noticeable effect, presumably because of the short duration of the calcium transients induced by these agents. Collagen-induced NFAT activation in megakaryocytes requires dephosphorylation by calcineurin and is completely sensitive to the calcineurin inhibitor cyclosporin A. Activation of NFAT by collagen was paralleled by the induction of the expression of Down Syndrome Critical Region I (DSCR1) and Fas Ligand (FasL), two genes recently identified as NFAT targets in megakaryocytes. Collagen-induced expression of DSCR1 and FasL occurred in a calcineurin- and NFAT-dependent manner, as it was blocked by both cyclosporin A as well as the specific peptide inhibitor of NFAT, VIVIT. These experiments show that the calcineurin pathway is a target for selected physiological ligands capable of inducing sustained calcium mobilization in megakaryocytes and regulates megakaryocyte gene expression in a cyclosporin A- and NFAT-dependent manner.

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

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