Practical Aspects of Measuring Intracellular Calcium Signals with Fluorescent Indicators

2010 ◽  
pp. 113-152 ◽  
Author(s):  
Joseph P.Y. Kao ◽  
Gong Li ◽  
Darryl A. Auston
Keyword(s):  
Intracellular Calcium ◽  
Calcium Signals ◽  
Fluorescent Indicators

Increased Aggregation and Secretion Responses of Human Platelets when Loaded with the Calcium Fluorescent Probes Quin2 and Fura-2

1987 ◽  
Vol 58 (02) ◽  
pp. 737-743 ◽  
Author(s):  
Frarnçois Lanza ◽  
Alain Beretz ◽  
Martial Kubina ◽  
Jean-Pierre Cazenave
Keyword(s):  
Intracellular Calcium ◽  
Shape Change ◽  
Calcium Ionophore ◽  
Human Platelets ◽  
Arachidonic Acid Metabolism ◽  
Free Calcium ◽  
Membrane Bilayer ◽  
Fluorescent Indicators ◽  
Fura 2 ◽  
Low Concentrations

SummaryIncorporation into human platelets of the calcium fluorescent indicators quin2 or fura-2 at low concentrations used to measure intracellular free calcium leads to the potentiation of the effects of agonists on platelets. This was shown by increased aggregatory and secretory responses of quin2 or fura-2 loaded platelets after stimulation with ADP, PAP and with low concentrations of thrombin, collagen, the endoperoxide analog U-46619 and the calcium ionophore A 23187. Quin2 and fura-2 mediated platelet sensitisation could be due to altered arachidonic acid metabolism since it was inhibited by prior treatment with the cydooxygenase inhibitor acetylsalicylate. In contrast, platelets loaded with higher concentrations of calcium chelators exhibited diminished aggregation responses to all aggregating agents. This latter effect was accompanied by increased fluidity of the platelet plasma membrane bilayer and by the exposure of a new pool of membranes to the outer surface of platelets, as monitored with trimethylammonium- diphenylhexatriene (TMA-DPH) in platelets loaded with the non-fluorescent calcium probe analog MAPT. In contrast, low concentrations of quin2 did not potentiate shape change of platelets activated with ADP. Thus, shape change and aggregation can be influenced separately by intracellular Ca2+ chelators. We conclude that platelet responses are altered by the incorporation of intracellular calcium chelators at concentrations used to monitor intracellular calcium changes.

Presynaptic calcium signals during neurotransmitter release: Detection with fluorescent indicators and other calcium chelators

1992 ◽  
Vol 86 (1-3) ◽  
pp. 129-134 ◽  
Author(s):  
GJ Augustine ◽  
EM Adler ◽  
MP Charlton ◽  
M Hans ◽  
D Swandulla ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Calcium Signals ◽  
Fluorescent Indicators ◽  
Presynaptic Calcium

Cerebral anoxia tolerance in turtles: regulation of intracellular calcium and pH

1992 ◽  
Vol 263 (6) ◽  
pp. R1298-R1302
Author(s):  
P. E. Bickler
Keyword(s):  
Intracellular Calcium ◽  
Brain Slices ◽  
Calcium Flux ◽  
Anoxia Tolerance ◽  
Acetoxymethyl Ester ◽  
Fluorescent Indicators ◽  
Cerebral Anoxia ◽  
Atp Production ◽  
Laboratory Rats ◽  
Inhibition Of Glycolysis

To investigate mechanisms of cerebral anoxia tolerance, cerebrocortical intracellular calcium ([Ca2+]i) and pH (pHi) regulation were compared in turtles (Trachemys scripta) and laboratory rats. [Ca2+]i and pHi in living 200 to 300-microns-thick cortical brain slices were measured with the fluorescent indicators fura-2/acetoxymethyl ester (AM) and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein during exposure to anoxia. Within 5 min, [Ca2+]i increased to > 1,000 nM in rat brain slices exposed to anoxia but [Ca2+]i was normal even after 5 h of anoxia in turtles. ATP levels remained normal in anoxic turtle brain but fell rapidly in rats. During anoxia, pHi fell by 0.25 +/- 0.08 pH units in rats but only 0.10 +/- 0.04 in turtles (P < 0.05). Inhibition of glycolysis in anoxic turtle brain with iodoacetate resulted in large increases in [Ca2+]i but prior exposure of slices to anoxia resulted in greatly attenuated calcium entry. The reduction in calcium flux was greater with increasing exposure to anoxia, suggesting progressive arrest of calcium channel activity. Tolerance of cerebral anoxia in turtles may be related to anaerobic ATP production, arrest of calcium channels, and attenuation of changes in pHi.

scholarly journals The BH4 domain of Bcl-XL rescues astrocyte degeneration in amyotrophic lateral sclerosis by modulating intracellular calcium signals

2011 ◽  
Vol 21 (4) ◽  
pp. 826-840 ◽  
Author(s):  
Francesca Martorana ◽  
Liliana Brambilla ◽  
Chiara F. Valori ◽  
Chiara Bergamaschi ◽  
Chiara Roncoroni ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Intracellular Calcium ◽  
Calcium Signals ◽  
Lateral Sclerosis

scholarly journals 168-03: Axial membrane tubules in atrial myocytes initiate rapid intracellular calcium signals through a new “super-hub” mechanism

EP Europace ◽  
2016 ◽  
Vol 18 (suppl_1) ◽  
pp. i114-i114
Author(s):  
Sören Brandenburg ◽  
Tobias Kohl ◽  
George S.b. Williams ◽  
Konstantin Gusev ◽  
Eva Wagner ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Atrial Myocytes ◽  
Calcium Signals ◽  
Membrane Tubules

Intracellular tetanic calcium signals are reduced in fatigue of whole skeletal muscle

1993 ◽  
Vol 264 (3) ◽  
pp. C577-C582 ◽  
Author(s):  
A. J. Baker ◽  
M. C. Longuemare ◽  
R. Brandes ◽  
M. W. Weiner
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Calcium Handling ◽  
Tetanic Stimulation ◽  
Muscle Contractility ◽  
Calcium Signals ◽  
Tetanic Force ◽  
Force Relaxation ◽  
Calcium Removal ◽  
Whole Muscle

Force and intracellular calcium signals were monitored in whole bullfrog semitendinosus muscles during fatigue produced by intermittent tetanic stimulation. Intracellular calcium signals were monitored using the fluorescent calcium-sensitive indicator indo-1 from the ratio of fluorescence intensities (R) at 400 and 470 nm. Fatiguing stimulation caused 1) proportional decreases of tetanic force and R, suggesting a component of the decreased force during fatigue of whole muscle may be due to insufficient calcium to activate contraction; 2) a progressive slowing of the relaxation of both force and R, suggesting slowed force relaxation may be mediated by slowed calcium removal from the myoplasm; 3) an increase of resting level R, suggesting impaired calcium removal from, or increased leakage to the cytosol; 4) prolongation of the twitch contraction, which was paralleled by changes in R. These findings are consistent with previous single fiber studies and suggest that changes in whole muscle contractility with fatigue may be partially mediated by changes in calcium handling by the cell.

Sign in / Sign up

Export Citation Format

Share Document