scholarly journals Hypotonically Induced Calcium Release from Intracellular Calcium Stores

1996 ◽  
Vol 271 (9) ◽  
pp. 4601-4604 ◽  
Author(s):  
Ludwig Missiaen ◽  
Humbert De Smedt ◽  
Jan B. Parys ◽  
Ilse Sienaert ◽  
Sara Vanlingen ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Stores ◽  
Intracellular Calcium Stores

Kinetic basis of quantal calcium release from intracellular calcium stores

Cell Calcium ◽  
1998 ◽  
Vol 23 (1) ◽  
pp. 43-52 ◽  
Author(s):  
LászlóG. Mészáros ◽  
Alexandra Zahradnikova ◽  
Pompeo Volpe
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Stores ◽  
Intracellular Calcium Stores

Intracellular calcium stores modulation in lymph vessels depends on wall stretch

1998 ◽  
Vol 76 (4) ◽  
pp. 367-372 ◽  
Author(s):  
D J Atchison ◽  
H Rodela ◽  
M G Johnston
Keyword(s):  
Intracellular Calcium ◽  
Vessel Wall ◽  
Calcium Release ◽  
Cyclopiazonic Acid ◽  
Transmural Pressure ◽  
Calcium Stores ◽  
Organ Bath ◽  
Intracellular Calcium Stores ◽  
Lymph Vessels ◽  
Calcium Induced Calcium Release

We studied the effect of intracellular calcium stores modulation on the ability of lymph vessels to propel fluid in a preparation of actively contracting isolated bovine mesenteric lymph vessels. Vessels were cannulated at each end, placed in a temperature-controlled organ bath, and circulated with oxygenated Krebs solution. Vessel wall tension (transmural pressure) was changed by raising the height of the fluid-filled reservoir and outflow catheters appropriately. When transmural pressure was set and maintained at 6 cmH2O (1 cmH2O = 98.1 Pa), caffeine (10-3 M), ryanodine (10-7 M), and cyclopiazonic acid (CPA; 7 x 10-6 M) inhibited lymphatic pumping. We also studied the effect of these agents on the relationship between lymph pump activity and transmural pressure, a relationship normally described by a bell-shaped curve. When transmural pressure was increased at 5-min intervals, the magnitude of inhibition by caffeine (10-3 M) and CPA (7 x 10-6 M) was greater than when transmural pressure was held constant. Ryanodine, on the other hand, had no effect on lymphatic contractility when transmural pressure was manipulated. The ryanodine results suggest the existence of an interaction between vessel wall stretch and intracellular calcium stores modulation that is not seen with caffeine or CPA.Key words: caffeine, ryanodine,cyclopiazonic acid, calcium-induced calcium release.

scholarly journals Impaired Calcium Release in Cerebellar Purkinje Neurons Maintained in Culture

2000 ◽  
Vol 115 (3) ◽  
pp. 339-346 ◽  
Author(s):  
Mary D. Womack ◽  
Jeffery W. Walker ◽  
Kamran Khodakhah
Keyword(s):  
Intracellular Calcium ◽  
Purkinje Cells ◽  
Calcium Release ◽  
Brain Slices ◽  
Purkinje Neurons ◽  
Calcium Stores ◽  
Intracellular Calcium Stores ◽  
Insp3 Receptors ◽  
Cerebellar Purkinje Neurons

Cerebellar Purkinje neurons demonstrate a form of synaptic plasticity that, in acutely prepared brain slices, has been shown to require calcium release from the intracellular calcium stores through inositol trisphosphate (InsP3) receptors. Similar studies performed in cultured Purkinje cells, however, find little evidence for the involvement of InsP3 receptors. To address this discrepancy, the properties of InsP3- and caffeine-evoked calcium release in cultured Purkinje cells were directly examined. Photorelease of InsP3 (up to 100 μM) from its photolabile caged analogue produced no change in calcium levels in 70% of cultured Purkinje cells. In the few cells where a calcium increase was detected, the response was very small and slow to peak. In contrast, the same concentration of InsP3 resulted in large and rapidly rising calcium responses in all acutely dissociated Purkinje cells tested. Similar to InsP3, caffeine also had little effect on calcium levels in cultured Purkinje cells, yet evoked large calcium transients in all acutely dissociated Purkinje cells tested. The results demonstrate that calcium release from intracellular calcium stores is severely impaired in Purkinje cells when they are maintained in culture. Our findings suggest that cultured Purkinje cells are an unfaithful experimental model for the study of the role of calcium release in the induction of cerebellar long term depression.

Presenilin-1 and intracellular calcium stores regulate neuronal glutamate uptake

2004 ◽  
Vol 88 (6) ◽  
pp. 1361-1372 ◽  
Author(s):  
Yaxiong Yang ◽  
Gregory A. Kinney ◽  
William J. Spain ◽  
John C. S. Breitner ◽  
David G. Cook
Keyword(s):  
Intracellular Calcium ◽  
Glutamate Uptake ◽  
Presenilin 1 ◽  
Calcium Stores ◽  
Intracellular Calcium Stores

scholarly journals Multiple Receptor Interactions Trigger Release of Membrane and Intracellular Calcium Stores Critical for Herpes Simplex Virus Entry

2007 ◽  
Vol 18 (8) ◽  
pp. 3119-3130 ◽  
Author(s):  
Natalia Cheshenko ◽  
Wen Liu ◽  
Lisa M. Satlin ◽  
Betsy C. Herold
Keyword(s):  
Herpes Simplex ◽  
Intracellular Calcium ◽  
Viral Entry ◽  
Calcium Stores ◽  
Calcium Response ◽  
Herpes Simplex Viruses ◽  
Intracellular Calcium Stores ◽  
Viral Binding ◽  
Glycoprotein H ◽  
Simplex Virus

Herpes simplex viruses (HSV) harness cellular calcium signaling pathways to facilitate viral entry. Confocal microscopy and small interfering RNA (siRNA) were used to identify the source of the calcium and to dissect the requisite viral–cell interactions. Binding of HSV to human epithelial cells induced no calcium response, but shifting the cells to temperatures permissive for penetration triggered increases in plasma membrane calcium followed by a global release of intracellular calcium. Transfection with siRNA targeting the proteoglycan syndecan-2 blocked viral binding and abrogated any calcium response. Transfection with siRNA targeting nectin-1, a glycoprotein D receptor, also prevented both membrane and intracellular calcium responses. In contrast, the membrane response was preserved after transfection with siRNA targeting integrinαv, a novel glycoprotein H receptor. The membrane response, however, was not sufficient for viral entry, which required interactions with integrinαv and release of inositol-triphosphate receptor-dependent intracellular calcium stores. Thus, calcium plays a critical, complex role in HSV entry.

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