Different characteristics of cell volume and intracellular calcium ion concentration dynamics between the hippocampal CA1 and lateral cerebral cortex of male mouse brain slices during exposure to hypotonic stress

2017 ◽  
Vol 96 (1) ◽  
pp. 117-127 ◽  
Author(s):  
Nanae Takahashi ◽  
Akibumi Omi ◽  
Hiroyuki Uchino ◽  
Yoshihisa Kudo
Keyword(s):  
Cerebral Cortex ◽  
Calcium Ion ◽  
Male Mouse ◽  
Brain Slices ◽  
Ion Concentration ◽  
Hypotonic Stress ◽  
Hippocampal Ca1 ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration ◽  
Different Characteristics

scholarly journals Platelet activating factor raises intracellular calcium ion concentration in macrophages.

1986 ◽  
Vol 103 (2) ◽  
pp. 439-450 ◽  
Author(s):  
G W Conrad ◽  
T J Rink
Keyword(s):  
Heavy Metals ◽  
Intracellular Calcium ◽  
Calcium Ion ◽  
Platelet Activating Factor ◽  
Ion Concentration ◽  
Early Event ◽  
Acetoxymethyl Ester ◽  
Intracellular Calcium Ion ◽  
The Times ◽  
Calcium Ion Concentration

Peritoneal cells from thioglycollate-stimulated mice were allowed to adhere to coverglasses for 2 h to give a dense monolayer of adherent cells greater than 95% of which were macrophages. After incubation with the tetra-acetoxymethyl ester of quin2, coverglasses were rinsed with Ca2+-free saline, oriented at a 45 degree angle in square cuvettes containing a magnetically driven stir bar, and analyzed for changes in quin2 fluorescence in a spectrofluorimeter. Such fluorescence, taken as an indication of intracellular calcium ion concentration ([Ca2+]i), increased as exogenous calcium ion concentration ([Ca2+]o) was raised to 1 mM. At [Ca2+]o approximately equal to 10 microM, [Ca2+]i = 72 +/- 14 nM (n = 26); at [Ca2+]o = 1 mM, [Ca2+]i = 140-220 nM, levels not increased by N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine, a membrane-permeant chelator of heavy metals than can quench quin2. Addition of mouse alpha + beta fibroblast interferon, lipopolysaccharide, thrombin, collagen, vasopressin, ADP, compound 48/80, or U46619 did not change [Ca2+]i. However, addition of platelet activating factor (PAF) (2-20 ng/ml) raised [Ca2+]i by 480 nM within 1 min if [Ca2+]o = 1 mM. In the presence of 5 mM EGTA, PAF raised [Ca2+]i by 25 nM. This suggests that PAF causes influx of exogenous Ca2+, as well as releasing some Ca2+ from intracellular stores. Consistent with these results, when PAF was added to 1 mM Ca2+ in the presence of 100 microM Cd2+ or Mn2+ to block Ca2+ influx, [Ca2+]i increased by only intermediate amounts; at the times of such dampened peak response, [Ca2+]i could be raised within 1 min to normal PAF-stimulated levels by chelation of the exogenous heavy metals with diethylenetriaminepentaacetic acid. Normal PAF responses were observed in the presence of indomethacin. The lowest dose of PAF observed to raise [Ca2+]i was 0.1 ng/ml. Response of [Ca2+]i to 2-20 ng/ml PAF was transient, and second applications had no effect. The PAF response also was seen in cell suspensions. These results suggest that an increase in [Ca2+]i may be an early event in PAF activation of macrophages.

scholarly journals Induction of Filopodia by Direct Local Elevation of Intracellular Calcium Ion Concentration

1999 ◽  
Vol 145 (6) ◽  
pp. 1265-1276 ◽  
Author(s):  
Pak-ming Lau ◽  
Robert S. Zucker ◽  
David Bentley
Keyword(s):  
Intracellular Calcium ◽  
Calcium Ion ◽  
Intracellular Signaling ◽  
Growth Cones ◽  
Ion Concentration ◽  
Rhodamine Phalloidin ◽  
Small Areas ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration ◽  
Neuronal Growth Cones

In neuronal growth cones, cycles of filopodial protrusion and retraction are important in growth cone translocation and steering. Alteration in intracellular calcium ion concentration has been shown by several indirect methods to be critically involved in the regulation of filopodial activity. Here, we investigate whether direct elevation of [Ca2+]i, which is restricted in time and space and is isolated from earlier steps in intracellular signaling pathways, can initiate filopodial protrusion. We raised [Ca2+]i level transiently in small areas of nascent axons near growth cones in situ by localized photolysis of caged Ca2+ compounds. After photolysis, [Ca2+]i increased from ∼60 nM to ∼1 μM within the illuminated zone, and then returned to resting level in ∼10–15 s. New filopodia arose in this area within 1–5 min, and persisted for ∼15 min. Elevation of calcium concentration within a single filopodium induced new branch filopodia. In neurons coinjected with rhodamine-phalloidin, F-actin was observed in dynamic cortical patches along nascent axons; after photolysis, new filopodia often emerged from these patches. These results indicate that local transient [Ca2+]i elevation is sufficient to induce new filopodia from nascent axons or from existing filopodia.

Rabbit cortical collecting ducts express a novel prostacyclin receptor

1995 ◽  
Vol 268 (1) ◽  
pp. F145-F154 ◽  
Author(s):  
R. L. Hebert ◽  
L. Regnier ◽  
L. N. Peterson
Keyword(s):  
Prostaglandin E2 ◽  
Calcium Ion ◽  
Collecting Duct ◽  
Ion Concentration ◽  
Cortical Collecting Duct ◽  
Water Conductivity ◽  
Prostacyclin Receptor ◽  
Collecting Ducts ◽  
Intracellular Calcium Ion ◽  
Calcium Ion Concentration

Prostaglandin E2 (PGE2) inhibits vasopressin-stimulated water conductivity (AVP-Lp) and inhibits Na+ reabsorption in the rabbit cortical collecting duct (CCD). Inhibition of Na+ reabsorption is mediated by increased intracellular calcium ion concentration ([Ca2+]i). Prostacyclin (PGI2) has also been shown to inhibit Na+ reabsorption in the CCD. The present studies were designed to examine the effect of the PGI2 agonist, Iloprost (ILP), on AVP-Lp and [Ca2+ in the isolated perfused rabbit CCD and to determine whether ILP activates different receptors than PGE2. ILP and PGE2 each maximally inhibited AVP-Lp equipotently at 10(-7) M. When CCDs were exposed to PGE2 and ILP simultaneously, or if PGE2 was added in the presence of ILP, inhibition of AVP-Lp was additive. Additivity was not observed if the PGI2 agonist, carbaprostacyclin (c-PGI2), was added with ILP, or if the PGE2 agonist, sulprostone, was added with PGE2, or if ILP was added to CCDs preexposed to PGE2. In fura 2-loaded CCD, ILP and PGE2 added separately increased [Ca2+]i. The response to c-PGI2 could be desensitized by prior exposure to ILP. ILP did not cause desensitization to PGE2, but PGE2 could desensitize the CCD to ILP. We conclude that PGI2 inhibits AVP-Lp by activation of a novel IP3 prostacyclin receptor and increases [Ca2+]i by activation of an IP1 prostacyclin receptor in the rabbit CCD. Functional evidence is presented that PGI2 cannot occupy PGE2 receptors and that PGE2 can occupy but cannot activate PGI2 receptors linked to inhibition of AVP-Lp.

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