scholarly journals Sustained increase in intracellular calcium promotes neuronal survival

1991 ◽  
Vol 11 (8) ◽  
pp. 2582-2587 ◽  
Author(s):  
F Collins ◽  
MF Schmidt ◽  
PB Guthrie ◽  
SB Kater
Keyword(s):  
Intracellular Calcium ◽  
Neuronal Survival ◽  
Sustained Increase

Increased Intracellular Calcium in Rat Anterior Piriform Cortex in Response to Threonine After Threonine Deprivation

1999 ◽  
Vol 81 (3) ◽  
pp. 1147-1149 ◽  
Author(s):  
Linda J. Magrum ◽  
M. Anne Hickman ◽  
Dorothy W. Gietzen
Keyword(s):  
Amino Acid ◽  
Intracellular Calcium ◽  
Piriform Cortex ◽  
Anterior Piriform Cortex ◽  
Enhanced Activity ◽  
Sustained Increase

Increased intracellular calcium in rat anterior piriform cortex in response to threonine after threonine deprivation The anterior piriform cortex (APC) may serve as the chemosensor for amino acid (AA) deficiency in rats. To investigate the mechanism by which the APC recognizes a limiting indispensable AA (IAA), we examined changes in intracellular calcium ([Ca2+]i) in APC slices after culture in medium with or without threonine (Thr) or lysine (Lys). The addition of 1 or 10 mM Thr to slices previously incubated in Thr-devoid medium resulted in a significant and sustained increase in [Ca2+]i compared to control slices; an effect not seen when isoleucine, another IAA, was added. Similar results were seen when lysine, but not threonine, was added to slices incubated in lysine-devoid medium. The rise in [Ca2+]iresulting from the addition of the limiting IAA to deficient slices may be linked to enhanced activity of the appropriate AA transporter. This is suggested by preliminary findings that serine, a small neutral AA that uses the same transporter as threonine, gave rise to an enhanced response in the Thr-deficient slice.

Volume regulation and intracellular calcium in the rabbit proximal convoluted tubule

1991 ◽  
Vol 260 (6) ◽  
pp. F861-F867 ◽  
Author(s):  
J. S. Beck ◽  
S. Breton ◽  
R. Laprade ◽  
G. Giebisch
Keyword(s):  
Intracellular Calcium ◽  
Cell Volume ◽  
Sodium Transport ◽  
Calcium Concentration ◽  
Basolateral Membrane ◽  
Potassium Conductance ◽  
Proximal Convoluted Tubule ◽  
Intracellular Calcium Concentration ◽  
Cell Swelling ◽  
Sustained Increase

The hypothesis that an increase of calcium leads to activation of calcium-activated ionic conductances during cell swelling was examined in the isolated perfused proximal convoluted tubule of the rabbit. Reduction of bath and luminal osmolality by 90 mosmol/kgH2O caused the cells to swell by 23.6 +/- 1.5% (n = 5) and intracellular calcium to rise from 227 +/- 35 to 347 +/- 60 nM (n = 6). Both these increases were transient, with volume decreasing to 5.5 +/- 1.2% above control and intracellular calcium concentration decreasing to 272 +/- 46 nM after 5-9 min. The addition of glucose and alanine to the tubule lumen to increase transcellular sodium transport caused a sustained increase in cell volume of 15.6 +/- 3.4% (n = 4). In parallel experiments, no significant increase in intracellular calcium concentration was observed. Addition of 1 microM of the calcium ionophore, ionomycin, reversibly increased intracellular calcium by 224 +/- 60 nM from a control value of 301 +/- 29 nM (n = 7) and reversibly depolarized the basolateral membrane by 3.6 +/- 0.9 mV (n = 5). However, there was no initial increase in the apparent transference number for potassium or chloride and no significant change in cell volume. We conclude from these observations that the sustained increase in basolateral potassium conductance observed when cells are swollen by hypotonicity or increased sodium transport (J. S. Beck and D. J. Potts. J. Physiol. Lond. 425: 369-378, 1990) is not due to a calcium-activated potassium conductance.

Effects of 17β-estradiol on intracellular calcium changes and neuronal survival after mechanical strain injury in neuronal–glial cultures

Synapse ◽  
2006 ◽  
Vol 60 (5) ◽  
pp. 406-410 ◽  
Author(s):  
Saitida Lapanantasin ◽  
Sukumal Chongthammakun ◽  
Candace L. Floyd ◽  
Robert F. Berman
Keyword(s):  
Intracellular Calcium ◽  
Neuronal Survival ◽  
Mechanical Strain ◽  
Glial Cultures ◽  
17Β Estradiol

Agonist-induced frequency modulation of Ca2+ oscillations in salt gland secretory cells

1991 ◽  
Vol 261 (1) ◽  
pp. C177-C184 ◽  
Author(s):  
K. M. Crawford ◽  
E. L. Stuenkel ◽  
S. A. Ernst
Keyword(s):  
Intracellular Calcium ◽  
Frequency Modulation ◽  
Calcium Concentration ◽  
Salt Gland ◽  
Effective Concentration ◽  
Secretory Cells ◽  
Oscillatory Frequency ◽  
Fura 2 ◽  
Dose Dependent ◽  
Sustained Increase

Oscillations in intracellular calcium concentration ([Ca2+]i) induced by the acetylcholine analogue carbachol (CCh) were characterized by microspectrofluorimetry of fura-2 in single secretory cells from the avian salt gland. The frequency of oscillations increased in graded fashion with [CCh] between 25 nM (2.7 +/- 0.6 min-1) and 250 nM (11.8 +/- 1.4 min-1), whereas the amplitude of the spikes was independent of [CCh]. An interperiod return to prestimulatory [Ca2+]i was generally seen only at very low (25 nM) CCh. Between 50 and 250 nM CCh, oscillations were associated with sustained elevated [Ca2+]i levels. The amplitude of the oscillatory spikes was found not to exceed that of initial spikes arising from prestimulatory [Ca2+]i, despite the dose-dependent [effective concentration at 50% (EC50) = 200 nM CCh] sustained rise in [Ca2+]i. At 1 microM CCh, oscillations gave way to a maximal sustained increase in [Ca2+]i. Reduction of [Ca2+]o to 1.5 microM during an oscillatory train or blockage of Ca2+ influx with Ni+ resulted in a reduction in sustained Ca2+i levels and in frequency, but not amplitude, of oscillations. A relationship between the sustained partial rise in [Ca2+]i derived from Ca2+ influx and the oscillatory frequency at a given [CCh] was further indicated by the lower frequency (P less than 0.01) of the early spikes in a train when interspike [Ca2+]i initially returned to near-basal levels. In some cells, oscillations were slow enough (less than 2 min-1) to resolve an interperiod of elevated baseline [Ca2+]i, showing that the latter can occur independent of the repetitive Ca2+ spikes. (ABSTRACT TRUNCATED AT 250 WORDS)

Presence of neuropeptide Y and the Y1 receptor in the plasma membrane and nuclear envelope of human endocardial endothelial cells: modulation of intracellular calcium

2003 ◽  
Vol 81 (3) ◽  
pp. 288-300 ◽  
Author(s):  
Danielle Jacques ◽  
Sawsan Sader ◽  
Claudine Perreault ◽  
Alain Fournier ◽  
Georges Pelletier ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Confocal Microscopy ◽  
Nuclear Envelope ◽  
Neuropeptide Y ◽  
Intracellular Calcium ◽  
Microscopy Technique ◽  
Human Fetal Heart ◽  
Endocardial Endothelial Cells ◽  
Npy Receptors ◽  
Sustained Increase

The aims of the present study were to investigate the presence and distribution of NPY and the Y1 receptor in endocardial endothelial cells (EECs), to verify if EECs can release NPY, and to determine if the effect of NPY on intracellular calcium is mediated via the Y1 receptor. Immunofluorescence, 3-D confocal microscopy and radioimmu noassay techniques were used on 20-week-old human fetal EECs. Our results showed that NPY and the Y1 receptor are present in human EECs (hEECs) and that their distributions are similar, the fluorescence labelling being higher in the nucleus and more particularly at the level of the nuclear envelope when compared with the cytosol. Using radio immunoassay, we demonstrated that EECs are a source of NPY and can secrete this peptide upon a sustained increase of intracellular calcium ([Ca]i). Using fluo-3 and 3-D confocal microscopy technique, superfusion of hEECs as well as EECs isolated from rat adult hearts with increasing concentrations of NPY induced a dose-dependent, sustained increase in free cytosolic and nuclear Ca2+ levels. This effect of NPY on EEC [Ca]i was completely reversible upon washout of NPY and was partially blocked by BIBP3226, a selective Y1 receptor antagonist. The results suggest that NPY and Y1 receptors are present in the EECs of 20-week-old human fetal heart and they share the same distribution and localization inside the cell. In addition, EECs are able to secrete NPY in response to an increase in [Ca]i, and the Y1 receptor as well as other NPY receptors seem to participate in mediating the effects of NPY on [Ca]i in these cells. Thus, NPY released by EECs may modulate excitation–secretion coupling of these cells.Key words: neuropeptide Y (NPY), nuclear envelope receptors, endocardial endothelial cells, NPY receptors, intracellular calcium.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.

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