Ca2+ dialogue between acidic vesicles and ER

2016 ◽  
Vol 44 (2) ◽  
pp. 546-553 ◽  
Author(s):  
Anthony J. Morgan
Keyword(s):  
Second Messengers ◽  
Secretory Vesicles ◽  
Ip3 Receptor ◽  
Inositol 1,4,5 Trisphosphate ◽  
Extracellular Stimuli ◽  
Acidic Vesicles ◽  
Lysosome Related Organelles ◽  
Intracellular Second Messengers ◽  
Global And Local ◽  
Signalling Cascade

Extracellular stimuli evoke the synthesis of intracellular second messengers, several of which couple to the release of Ca2+ from Ca2+-storing organelles via activation of cognate organellar Ca2+-channel complexes. The archetype is the inositol 1,4,5-trisphosphate (IP3) and IP3 receptor (IP3R) on the endoplasmic reticulum (ER). A less understood, parallel Ca2+ signalling cascade is that involving the messenger nicotinic acid adenine dinucleotide phosphate (NAADP) that couples to Ca2+ release from acidic Ca2+ stores [e.g. endo-lysosomes, secretory vesicles, lysosome-related organelles (LROs)]. NAADP-induced Ca2+ release absolutely requires organellar TPCs (two-pore channels). This review discusses how ER and acidic Ca2+ stores physically and functionally interact to generate and shape global and local Ca2+ signals, with particular emphasis on the two-way dialogue between these two organelles.

Modulation of signalling initiated by phosphoinositidase-C-linked receptors

1993 ◽  
Vol 184 (1) ◽  
pp. 145-159
Author(s):  
R. J. Wojcikiewicz ◽  
S. R. Nahorski
Keyword(s):  
Cell Surface ◽  
Second Messengers ◽  
Receptor Internalization ◽  
Intensive Study ◽  
Receptor Stimulation ◽  
Surface Receptors ◽  
Regulatory Processes ◽  
Inositol 1,4,5 Trisphosphate ◽  
Cellular Responsiveness ◽  
Intracellular Second Messengers

An extensive group of cell surface receptors are coupled to phosphoinositidase C and thus to the production of the intracellular second messengers inositol 1,4,5-trisphosphate and 1,2-diacylglycerol. While the mechanisms and consequences of phosphoinositidase C activation have been the target of intensive study for over a decade, information is scarce regarding the regulatory processes that modulate this system during receptor stimulation. This situation, however, is now beginning to change. Recent data indicate (a) that Ca2+, mobilized concurrently with activation of phosphoinositidase-C-linked receptors, is a feedback activator and amplifier of phosphoinositide hydrolysis, (b) that rapid desensitization, possibly associated with receptor phosphorylation, regulates phosphoinositidase-C-linked receptors, (c) that receptor internalization can mediate desensitization at later times and (d) that signalling can be regulated at additional sites downstream of phosphoinositidase C. These diverse regulatory events provide the means by which the breakdown of phosphoinositides and cellular responsiveness to their products are controlled during cell stimulation.

scholarly journals Differential regulation of nicotinic acid–adenine dinucleotide phosphate and cADP-ribose production by cAMP and cGMP

1998 ◽  
Vol 331 (3) ◽  
pp. 837-843 ◽  
Author(s):  
Heather L. WILSON ◽  
Antony GALIONE
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Calcium Release ◽  
Second Messengers ◽  
Differential Regulation ◽  
Sea Urchin Egg ◽  
Inositol 1,4,5 Trisphosphate ◽  
Extracellular Stimuli ◽  
Camp And Cgmp ◽  
Temperature Optima

The sea urchin egg has been used as a system to study calcium-release mechanisms induced by inositol 1,4,5-trisphosphate (IP3), cADP-ribose (cADPR), and more recently, nicotinic acid–adenine dinucleotide phosphate (NAADP). In order that cADPR and NAADP may be established as endogenous messengers for calcium release, the existence of intracellular enzymes capable of metabolizing these molecules must be demonstrated. In addition, intracellular levels of cADPR and NAADP should be under the control of extracellular stimuli. It has been shown that cGMP stimulates the synthesis of cADPR in the sea urchin egg. The present study shows that the sea urchin egg is capable of synthesizing and degrading NAADP. cADPR and NAADP synthetic activities appear to be separate, with different cellular localizations, pH and temperature optima. We suggest that in the sea urchin egg, cADPR and NAADP production may be differentially regulated by receptor-coupled second messengers, with cADPR production being regulated by cGMP and NAADP production modulated by cAMP.

Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels

1998 ◽  
Vol 78 (1) ◽  
pp. 53-97 ◽  
Author(s):  
FRANK M. FARACI ◽  
DONALD D. HEISTAD
Keyword(s):  
Potassium Channels ◽  
Cerebral Circulation ◽  
Second Messengers ◽  
Chronic Hypertension ◽  
Major Mechanism ◽  
Disease States ◽  
Vasoactive Factors ◽  
New Concepts ◽  
Intracellular Second Messengers

Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.

PACAP38 Modulates Activity of NMDA Receptors in Cultured Chick Cortical Neurons

1997 ◽  
Vol 78 (4) ◽  
pp. 2231-2234 ◽  
Author(s):  
Guo Jun Liu ◽  
Barry W. Madsen
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Cortical Neurons ◽  
Second Messengers ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Low Concentrations ◽  
Channel Opening ◽  
Pituitary Adenylate Cyclase ◽  
Intracellular Second Messengers

Liu, Guo Jun and Barry W. Madsen. PACAP38 modulates activity of NMDA receptors in cultured chick cortical neurons. J. Neurophysiol. 78: 2231–2234, 1997. The outside-out recording mode of the patch-clamp technique was used to study modulatory effects of pituitary adenylate cyclase-activating polypeptide (PACAP38) on N-methyl-d-aspartate (NMDA) receptor activity in cultured chick cortical neurons. Biphasic concentration-dependent effects of PACAP38 on channel opening frequency induced by NMDA (20 μM) and glycine (1 μM) were found, with low concentrations (0.5–2 nM) of PACAP38 increasing activity and higher concentrations (10–1,000 nM) causing inhibition. These effects were reversible, reduced with higher concentrations of glycine (2–10 μM) but not by 200 μM NMDA, and inhibited by 10 μM 7-chlorokynurenic acid. In addition, 1 μM PACAP6–38 (a PACAP antagonist) inhibited channel activity due to 20 μM NMDA and 1 μM glycine by 66%, and this inhibition was reduced to 13% in the additional presence of 2 nM PACAP38. These observations suggest thatPACAP38 has a direct modulatory effect on the NMDA receptor that is independent of intracellular second messengers and probably mediated through the glycine coagonist site(s).

The existence of inositol 1,4,5-trisphosphate and ryanodine receptors in mature bovine oocytes

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2645-2654 ◽  
Author(s):  
C. Yue ◽  
K.L. White ◽  
W.A. Reed ◽  
T.D. Bunch
Keyword(s):  
Ryanodine Receptors ◽  
Inhibitory Effect ◽  
Ruthenium Red ◽  
Calcium Oscillations ◽  
Ip3 Receptor ◽  
Cyclic Adp Ribose ◽  
Inositol 1,4,5 Trisphosphate ◽  
Bovine Oocytes ◽  
Continuous Injection

Intracellular Ca2+ (Ca2+i) transients during fertilization are critical to the activation of eggs in all species studied. Activation of both the inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) and ryanodine receptor (RYR) are responsible for the calcium oscillations during fertilization in sea urchin eggs. Using in vitro matured bovine oocytes loaded with Fura-2 AM ester as Ca2+i indicator, we addressed whether IP3Rs and RYRs coexist in mammalian eggs. Our results indicate that microinjection of 50–250 nM IP3 or 10–20 mM caffeine, 100–200 microM ryanodine and 4–8 microM cyclic ADP-ribose all induced Ca2+i release. The Ca2+i release induced by 250 nM IP3 could only be inhibited by prior injection of 1 mg/ml heparin which was overcome by continuous injection of IP3 to 1 microM. Prior injection of either 50 microM ruthenium red, 50 microM procaine or 1 % vehicle medium (VM) did not affect the Ca2+i release induced by IP3. Prior injection of heparin or VM did not affect the Ca2+i release induced by 10–20 mM caffeine or 200 microM ryanodine, but prior injection of 50 microM ruthenium red or procaine completely inhibited the effect of 10–20 mM caffeine. In addition, continuous injection of caffeine up to 40 mM overcame the inhibitory effect of ruthenium red or procaine. The same 50 microM concentration of ruthenium red or procaine only partially blocked the effect of 200 microM ryanodine, but 200 microM ruthenium red or procaine completely blocked the effect of 200 microM ryanodine.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document