scholarly journals Intracellular calcium and cyclic nucleotide levels modulate neurite guidance by microtopographical substrate features

2016 ◽  
Vol 104 (8) ◽  
pp. 2037-2048 ◽  
Author(s):  
Shufeng Li ◽  
Bradley Tuft ◽  
Linjing Xu ◽  
Marc Polacco ◽  
Joseph C. Clarke ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Cyclic Nucleotide ◽  
Neurite Guidance

Differential effects of intracellular calcium elevating agents on adrenergic-stimulated cyclic nucleotide and melatonin synthesis in rat pinealocytes

1992 ◽  
Vol 70 (9) ◽  
pp. 1254-1260 ◽  
Author(s):  
Anthony K. Ho ◽  
Joshua Cheng ◽  
Marc Girard
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Intracellular Calcium ◽  
Cyclic Nucleotide ◽  
Melatonin Synthesis ◽  
Kinase C ◽  
Mechanism Of Inhibition ◽  
Intracellular Ca

In this study, the role of elevation of intracellular Ca2+ and activation of protein kinase C on adrenergic-stimulated cyclic nucleotide accumulation and melatonin synthesis in rat pinealocytes was investigated. It was found that whereas KCl, ionomycin, and ouabain, three Ca2+-elevating agents, had a potentiating effect on adrenergic-stimulated cylic AMP response, their effects on melatonin synthesis were inhibitory. Similar inhibition was also observed when dibutyryl cyclic AMP was used to stimulate melatonin synthesis. By determining intracellular Ca2+ directly, it was found that the enhancing effects of these agents on the cyclic AMP response but not their inhibitory effects on melatonin synthesis paralleled their abilities to elevate intracellular Ca2+. In comparison, activation of protein kinase C significantly enhanced the adrenergic-stimulated cyclic AMP response and, to a lesser degree, the adrenergic-stimulated N-acetyltransferase and melatonin levels. These results indicate that (i) Ca2+-elevating agents have opposite effects on adrenergic-stimulated cyclic AMP and melatonin production; (ii) a post cyclic AMP event of importance to melatonin synthesis is inhibited by these agents; and (iii) the mechanism of inhibition may not be directly related to their effect on intracellular Ca2+.Key words: intracellular calcium, protein kinase C, melatonin, pineal gland.

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.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.

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