Calcium currents of differentiated mouse neuroblastoma cells

1985 ◽  
Vol 16 (4) ◽  
pp. 419-422
Author(s):  
N. S. Veselovskii ◽  
N. Kh. Pogorelaya ◽  
A. F. Fomina
Keyword(s):  
Neuroblastoma Cells ◽  
Calcium Currents ◽  
Mouse Neuroblastoma

scholarly journals Two components of voltage-dependent calcium influx in mouse neuroblastoma cells. Measurement with arsenazo III.

1986 ◽  
Vol 88 (2) ◽  
pp. 149-165 ◽  
Author(s):  
S R Bolsover
Keyword(s):  
Intracellular Calcium ◽  
Calcium Current ◽  
Calcium Influx ◽  
Neuroblastoma Cells ◽  
Calcium Currents ◽  
Arsenazo Iii ◽  
Optical Absorbance ◽  
Mouse Neuroblastoma ◽  
Calcium Indicator ◽  
Voltage Dependent

N1E-115 mouse neuroblastoma cells were injected with the calcium indicator dye arsenazo III. Optical absorbance changes during voltage-clamp depolarization were used to examine the properties of the two calcium currents present in these cells. The rapidly inactivating calcium current (Moolenar and Spector, 1979b, Journal of Physiology, 292:307-323) inactivates by a voltage-dependent mechanism. The slowly inactivating calcium current is dominant in raising intracellular calcium during depolarizations to greater than -20 mV. Lowering the extracellular calcium concentration affects the two calcium currents unequally, with the slowly inactivating current being reduced more. Intracellular calcium falls very slowly (tau greater than 1 min) after a depolarization. The rapidly inactivating calcium current is responsible for a calcium action potential under physiological conditions. In contrast, it is unlikely that the slowly inactivating calcium current has an important electrical role. Rather, its function may be to add a further increment of calcium influx over and above the calcium influx through the rapidly inactivating calcium channels.

On the Application of Cultured Neuronal Cell Lines in Neurotoxicological Studies: Cytotoxicity of Acrylamide

1983 ◽  
Vol 11 (3) ◽  
pp. 135-145
Author(s):  
Erik Walum
Keyword(s):  
Cell Lines ◽  
Culture Medium ◽  
Neuroblastoma Cells ◽  
Neuronal Cell ◽  
Leucine Incorporation ◽  
Biochemical Process ◽  
Neurite Retraction ◽  
Mouse Neuroblastoma ◽  
Neuronal Cell Lines

Summary Acrylamide, a well known neurotoxic compound, was used in a first evaluation of cultured mouse neuroblastoma cells as an alternative to animal models for neurotoxicological studies. Hence, the effects of acrylamide on the growth, size, morphology and leucine incorporation of three neuroblastoma (41A3, N18 and N1E115), one neuroblastoma x glioma hybrid (NG108CC15), two glioma (138MG and C6) and two fibroblast (RLF and RMC) cell lines were studied. It was found that the concentration of acrylamide needed to inhibit the growth by 50% in 24 hr was similar in all cell lines, i.e. around 2 x 10-4g/ml culture medium. In the two cell lines, N1E115 and NG108CC15, acrylamide at this concentration caused neurite retraction and at higher concentrations (5 x 10-4g/ml) a decrease in cell viability. In a concentration range of 5 x 10-5 - 5 x 10-4g/ml acrylamide did not affect cell size, or at 2 x 10-4g/ml incorporation of leucine into trichloroacetic acid precipitable material. It is suggested that acrylamide interferes with a biochemical process common to all the tested cells, but of greater importance in differentiated nerve cells than in others. Whether this process is consistent with the in vivo target for the neurotoxic action of acrylamide remains to be unravelled.

Ultrastructure of multiple microtubule initiation sites in mouse neuroblastoma cells

1981 ◽  
Vol 47 (1) ◽  
pp. 1-24
Author(s):  
G.A. Sharp ◽  
M. Osborn ◽  
K. Weber
Keyword(s):  
Electron Microscopy ◽  
Electron Microscope ◽  
Immunofluorescence Microscopy ◽  
Neuroblastoma Cells ◽  
Biological Significance ◽  
Optimal Conditions ◽  
Serial Sectioning ◽  
Mouse Neuroblastoma ◽  
Microtubule Organizing Centres ◽  
Perinuclear Area

Morphologically undifferentiated and differentiated mouse neuroblastoma N115 and N18 cells were examined after serial sectioning by electron microscopy. A sizeable percentage of the cells revealed multiple centrioles, usually clustered together in the perinuclear area with 2 preferential locations, i.e. above and below the largest nuclear diameter. These results indicate that the multiple microtubule-organizing centres previously visualized by immunofluorescence microscopy with tubulin antibody in neuroblastoma cells recovering from Colcemid poisoning are most likely in majority related to multiple centrioles. This interpretation is further strengthened by experiments in which cells are first recorded in the fluorescence microscope and then after serial sectioning in the electron microscope. The results show that under optimal conditions immunofluorescence microscopy is able to visualize single centrioles. The possible biological significance of the combined electron and immunofluorescence microscopical results is discussed.

scholarly journals Modulation of calcium signaling depends on the oligosaccharide of GM1 in Neuro2a mouse neuroblastoma cells

2020 ◽  
Vol 37 (6) ◽  
pp. 713-727
Author(s):  
Giulia Lunghi ◽  
Maria Fazzari ◽  
Erika Di Biase ◽  
Laura Mauri ◽  
Sandro Sonnino ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Calcium Channels ◽  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Calcium Imaging ◽  
Neuroblastoma Cells ◽  
Ganglioside Gm1 ◽  
Mouse Neuroblastoma ◽  
Neuro2a Cells ◽  
Neuronal Functions

AbstractRecently, we demonstrated that the oligosaccharide portion of ganglioside GM1 is responsible, via direct interaction and activation of the TrkA pathway, for the ability of GM1 to promote neuritogenesis and to confer neuroprotection in Neuro2a mouse neuroblastoma cells. Recalling the knowledge that ganglioside GM1 modulates calcium channels activity, thus regulating the cytosolic calcium concentration necessary for neuronal functions, we investigated if the GM1-oligosaccharide would be able to overlap the GM1 properties in the regulation of calcium signaling, excluding a specific role played by the ceramide moiety inserted into the external layer of plasma membrane. We observed, by calcium imaging, that GM1-oligosaccharide administration to undifferentiated Neuro2a cells resulted in an increased calcium influx, which turned out to be mediated by the activation of TrkA receptor. The biochemical analysis demonstrated that PLCγ and PKC activation follows the TrkA stimulation by GM1-oligosaccharide, leading to the opening of calcium channels both on the plasma membrane and on intracellular storages, as confirmed by calcium imaging experiments performed with IP3 receptor inhibitor. Subsequently, we found that neurite elongation in Neuro2a cells was blocked by subtoxic administration of extracellular and intracellular calcium chelators, suggesting that the increase of intracellular calcium is responsible of GM1-oligosaccharide mediated differentiation. These results suggest that GM1-oligosaccharide is responsible for the regulation of calcium signaling and homeostasis at the base of the neuronal functions mediated by plasma membrane GM1.

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