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.

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

Structure and function of the neuronal endomembrane system

1993 ◽  
Vol 51 ◽  
pp. 98-99
Author(s):  
Maryann E. Martone ◽  
Victoria M. Simpliciano ◽  
Ying Zhang ◽  
Thomas J. Deerinck ◽  
Mark H. Ellisman
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Smooth Endoplasmic Reticulum ◽  
Ryanodine Receptors ◽  
Cell Types ◽  
Calcium Stores ◽  
Endomembrane System ◽  
Ip3 Receptor ◽  
And Function ◽  
Cerebellar Purkinje Neurons

Components of the endomembrane system in a variety of cell types appear to function in the storage and release of calcium similar to the muscle sarcoplasmic reticulum. Many proteins involved in intracellular calcium regulation in skeletal or smooth muscle, e.g. Ca++ ATPase, calsequestrin, the inositol l,4,5,trisphosphate (TP3) receptor and the ryanodine binding protein, are found in the nervous system where they are particularly abundant within the smooth endoplasmic reticulum (SER) of cerebellar Purkinje neurons. Immunolocalization studies suggest, however, that calcium regulatory proteins are not uniformly distributed within the SER but are concentrated in or excluded from certain domains. For example, the IP3 and ryanodine receptors, two distinct calcium channels which mediate calcium release by different ligands, are found associated with the SER in cell bodies and dendrites of chick cerebellum but only the IP3 receptor is found within dendritic spines. These results are consistent with evidence that cells may possess multiple intracellular calcium stores that are pharmacologically, spatially and perhaps physically distinct.

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

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 Junctate is a key element in calcium entry induced by activation of InsP3 receptors and/or calcium store depletion

2004 ◽  
Vol 166 (4) ◽  
pp. 537-548 ◽  
Author(s):  
Susan Treves ◽  
Clara Franzini-Armstrong ◽  
Luca Moccagatta ◽  
Christophe Arnoult ◽  
Cristiano Grasso ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Binding ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Receptor Activation ◽  
Calcium Entry ◽  
Calcium Stores ◽  
Store Depletion ◽  
Insp3 Receptors

In many cell types agonist-receptor activation leads to a rapid and transient release of Ca2+ from intracellular stores via activation of inositol 1,4,5 trisphosphate (InsP3) receptors (InsP3Rs). Stimulated cells activate store- or receptor-operated calcium channels localized in the plasma membrane, allowing entry of extracellular calcium into the cytoplasm, and thus replenishment of intracellular calcium stores. Calcium entry must be finely regulated in order to prevent an excessive intracellular calcium increase. Junctate, an integral calcium binding protein of endo(sarco)plasmic reticulum membrane, (a) induces and/or stabilizes peripheral couplings between the ER and the plasma membrane, and (b) forms a supramolecular complex with the InsP3R and the canonical transient receptor potential protein (TRPC) 3 calcium entry channel. The full-length protein modulates both agonist-induced and store depletion–induced calcium entry, whereas its NH2 terminus affects receptor-activated calcium entry. RNA interference to deplete cells of endogenous junctate, knocked down both agonist-activated calcium release from intracellular stores and calcium entry via TRPC3. These results demonstrate that junctate is a new protein involved in calcium homeostasis in eukaryotic cells.

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