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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study outlines the effects of a modification of the actin-based cytoskeleton on the maturation of rabies virus in human neuroblastoma cell and primary rat cortical neuron cultures. In a Ca(2+)-depleted or an EGTA-containing medium, disruption of microfilaments did not affect intracellular viral nucleoprotein synthesis, as demonstrated by dual-immunofluorescence microscopy, and caused no change in the extracellular titre of rabies virus. Furthermore, the continuous presence of the anti-calmodulin drugs trifluoperazine (1 to 20 microM) and chlorpromazine (1 to 30 microM), or the L-type Ca2+ channel antagonist nifedepine (1 to 10 microM) or the Ca(2+)-specific ionophore A23187 (0.05 to 1.0 microM), did not modify the extracellular titre of rabies virus significantly over a 48 h period. The inference from these studies is that the maturation of rabies virus is independent of the integrity of the microfilament structures and calmodulin-dependent processes of neuronal cells.
J Gen Virol 1991 Sep
PMID:Actin-independent maturation of rabies virus in neuronal cultures. 189 64

Currents through sodium channels of neuroblastoma cells were measured using patch technique in outside-out configuration. Scorpion toxin (ScTX) produced 3 to 4 fold prolongation of mean open time and increased number of reopenings. The mean open times showed slow fluctuations around some average values. The distribution of channel open times for ScTX-modified channels required more than one exponential to be fitted. Chloramine-T (ChT) produced qualitatively similar, though weaker, prolongation of open times.
Gen Physiol Biophys 1990 Feb
PMID:Some properties of sodium channels in neuroblastoma cells modified with scorpion toxin and chloramine-T. Single channel measurements. 215 49

Single sodium channel events were recorded from cell-attached patches on single canine cardiac Purkinje cells at 10-13 degrees C. Data from four patches containing two to four channels and one patch with one channel were selected for quantitative analysis. The channels showed prominent reopening behavior at voltages near threshold, and the number of reopenings declined steeply with depolarization. Mean channel open time was a biphasic function of voltage with the maximum value (1-1.5 ms) occurring between -50 and -40 mV and lower values at more and at less hyperpolarized levels. Inactivation without opening was also prominent near threshold, and this occurrence also declined with depolarization. The waiting time distributions and the probability of being open showed voltage and time dependence as expected from whole-cell current studies. The results were analyzed in terms of a five-state Markovian kinetic model using both histogram analysis and a maximum likelihood method to estimate kinetic parameters. The kinetic parameters of the model fits were similar to those of GH3 pituitary cells (Horn, R., and C. A. Vandenberg. 1984. Journal of General Physiology. 84:505-534) and N1E115 neuroblastoma cells (Aldrich, R. W., and C. F. Stevens. Journal of Neuroscience. 7:418-431). Both histogram and maximum likelihood analysis implied that much of the voltage dependence of cardiac Na current is in its activation behavior, with inactivation showing modest voltage dependence.
J Gen Physiol 1990 Mar
PMID:Kinetic analysis of single sodium channels from canine cardiac Purkinje cells. 215 91

Aconitine-modified sodium channels in the neuroblastoma cell membrane were investigated with patch-clamp technique in outside-out configuration. When aconitine (0.1 mmol/l) was present in the pipette solution two types of modified single sodium channels were observed. The first type showed openings with normal amplitude (slope conductance 15.5 pS) and bursting behaviour. The second type of modified channel openings was characterized with low amplitude (slope conductance 2.8 pS) and longer open time as comparing to unmodified channels. The low-amplitude channels were shown to have altered ion selectivity: they were permeable to NH4+. Both populations of aconitine-modified channels could be blocked by tetrodotoxin. In contrast to macroscopic current experiments (Mozhayeva et al. 1977) the development of aconitine modification was not affected by repetitive stimulation and external application of the agent had no effect on single sodium channels in outside-out membrane patch.
Gen Physiol Biophys 1990 Apr
PMID:Aconitine-induced modification of single sodium channels in neuroblastoma cell membrane. 216 97

Ionic currents induced by 5-hydroxytryptamine (5-HT) in cultured neuroblastoma N18 cells were studied using whole-cell voltage clamp. The response was blocked by 1-10 nM 5-HT3 receptor-specific antagonists MDL 7222 or ICS 205-930, but not by 1 microM 5-HT1/5-HT2 receptor antagonist spiperone or 5-HT2 receptor-specific antagonist ketanserin. These 5-HT3 receptors seem to be ligand-gated channels because the response (a) did not require internal ATP or GTP, (b) persisted with long internal dialysis of CsF (90 mM), A1F4- (100 microM), or GTP gamma S (100 microM), and (c) with ionophoretic delivery of 5-HT developed with a delay of less than 10 ms and rose to a peak in 34-130 ms. Fluctuation analysis yielded an apparent single-channel conductance of 593 fS. The relative permeabilities of the channel for a variety of ions were determined from reversal potentials. The channel was only weakly selective among small cations, with permeability ratios PX/PNa of 1.22, 1.10, 1.01, 1.00, and 0.99 for Cs+, K+, Li+, Na+, and Rb+, and 1.12, 0.79, and 0.73 for Ca2+, Ba2+, and Mg2+ (when studied in mixtures of 20 mM divalent ions and 120 mM N-methyl-D-glucamine). Apparent permeability ratios for the divalent ions decreased as the concentration of divalent ions was increased. Small monovalent organic cations were highly permeant. Large organic cations such as Tris and glucosamine were measurably permeant with permeability ratios of 0.20 and 0.08, and N-methyl-D-glucamine was almost impermeant. Small anions, NO3-, Cl-, and F-, were slightly permeant with permeability ratios of 0.08, 0.04, and 0.03. The results indicate that the open 5-HT3 receptor channel has an effective minimum circular pore size of 7.6 A and that ionic interactions in the channel may involve negative charges near the pore mouth.
J Gen Physiol 1990 Dec
PMID:Ion permeation through 5-hydroxytryptamine-gated channels in neuroblastoma N18 cells. 228 32

Sodium and calcium inward currents (INa and ICa) were measured in neuroblastoma X glioma hybrid cells of clones 108CC5 and 108CC15 by a single suction pipette method for internal perfusion and voltage clamp. Morphologically undifferentiated, exponentially growing cells were compared with cells differentiated by cultivation with 1 mmol/l dibutyryl cyclic AMP. Outward currents were eliminated by perfusing the cells with a K+-free solution. Voltage dependence and ion selectivity as well as steady state inactivation characteristics of INa and ICa resembled those of differentiated mouse neuroblastoma cells, clone N1E-115 (Moolenaar and Spector 1978, 1979). These parameters were identical in undifferentiated and differentiated cells of both clones. After differentiation the average density of the peak sodium and calcium currents was increased two and four-fold, respectively, in both cell lines. Our data indicate that exponentially growing, morphologically undifferentiated 108CC5 and 108CC15 neuroblastoma X glioma hybrid cells possess functional Na+ and Ca2+ channels undistinguishable from those of non-proliferating cells of these clones differentiated morphologically by treatment with dibutyryl cyclic AMP. That Na+ and Ca2+ spikes were not detected by other authors in these cells prior to morphological differentiation by dibutyryl cyclic AMP may be attributed to the fact that at the low resting membrane potential measured the Na+ and Ca2+ channels are inactivated.
Gen Physiol Biophys 1985 Apr
PMID:Sodium and calcium currents in neuroblastoma x glioma hybrid cells before and after morphological differentiation by dibutyryl cyclic AMP. 241 25

The kinetics of activation and inactivation of the inward calcium current (ICa) in morphologically undifferentiated and differentiated neuroblastoma X glioma hybrid cells of the clone 108CC15 were studied by the suction pipette technique for internal perfusion and voltage clamping. Potassium currents were eliminated by internal perfusion of the cells with a K+-free solution. Activation of ICa followed a sigmoidal time course and could reasonably be fitted by a m2 relation. The kinetics of ICa inactivation were studied by analyzing the current inactivation during long depolarizing steps and by measuring the peak ICa as a function of the length of a prepulse. Both methods gave comparable results indicating that the ICa inactivation cannot be fitted by a single exponential. The ICa inactivation was fitted by a biexponential function. Neither the activation nor the inactivation of ICa were changed after morphological cell differentiation induced by treatment with dibutyryl cyclic AMP.
Gen Physiol Biophys 1985 Apr
PMID:A kinetic analysis of the inward calcium current in 108CC15 neuroblastoma x glioma hybrid cells. 241 26

Single channel currents of sodium channels purified from rat brain and reconstituted into planar lipid bilayers were recorded. The kinetics of channel gating were investigated in the presence of batrachotoxin to eliminate inactivation and an analysis was conducted on membranes with a single active channel at any given time. Channel opening is favored by depolarization and is strongly voltage dependent. Probability density analysis of dwell times in the closed and open states of the channel indicates the occurrence of one open state and several distinct closed states in the voltage (V) range-120 mV less than or equal to V less than or equal to +120 mV. For V less than or equal to 0, the transition rates between stages are exponentially dependent on the applied voltage, as described in mouse neuroblastoma cells (Huang, L. M., N. Moran, and G. Ehrenstein. 1984. Biophysical Journal. 45:313-322). In contrast, for V greater than or equal to 0, the transition rates are virtually voltage independent. Autocorrelation analysis (Labarca, P., J. Rice, D. Fredkin, and M. Montal. 1985. Biophysical Journal. 47:469-478) shows that there is no correlation in the durations of successive open or closing events. Several kinetic schemes that are consistent with the experimental data are considered. This approach may provide information about the mechanism underlying the voltage dependence of channel activation.
J Gen Physiol 1986 Jul
PMID:Sodium channels in planar lipid bilayers. Channel gating kinetics of purified sodium channels modified by batrachotoxin. 242 88

Macroscopic Na currents were recorded from N18 neuroblastoma cells by the whole-cell voltage-clamp technique. Inactivation of the Na currents was removed by intracellular application of proteolytic enzymes, trypsin, alpha-chymotrypsin, papain, or ficin, or bath application of N-bromoacetamide. Unlike what has been reported in squid giant axons and frog skeletal muscle fibers, these treatments often increased Na currents at all test pulse potentials. In addition, removal of inactivation gating shifted the midpoint of the peak Na conductance-voltage curve in the negative direction by 26 mV on average and greatly prolonged the rising phase of Na currents for small depolarizations. Polypeptide toxins from Leiurus quinquestriatus scorpion and Goniopora coral, which slow inactivation in adult nerve and muscle cells, also increase the peak Na conductance and shift the peak conductance curve in the negative direction by 7-10 mV in neuroblastoma cells. Control experiments argue against ascribing the shifts to series resistance artifacts or to spontaneous changes of the voltage dependence of Na channel kinetics. The negative shift of the peak conductance curve, the increase of peak Na currents, and the prolongation of the rise at small depolarization after removal of inactivation are consistent with gating kinetic models for neuroblastoma cell Na channels, where inactivation follows nearly irreversible activation with a relatively high, voltage-independent rate constant and Na channels open only once in a depolarization. As the same kind of experiment does not give apparent shifting of activation and prolongation of the rising phase of Na currents in adult axon and muscle membranes, the Na channels of these other membranes probably open more than once in a depolarization.
J Gen Physiol 1987 Feb
PMID:Gating of Na channels. Inactivation modifiers discriminate among models. 243 40

Monoclonal antibodies (MAbs) specific for the rabies virus nucleoprotein (N protein) and non-structural (NS) protein of the nucleocapsid were introduced into adherent cells (fibroblasts and neuroblastoma) by the scrape-loading technique. After the cells had reattached to the substrate, they were infected with rabies virus. Inhibition of infection was monitored by measuring the intracytoplasmic viral nucleocapsid accumulation with an enzyme immunoassay using anti-N protein rabbit serum and by measuring the release of infectious virus with the plaquing system. Seventeen MAbs defining the three independent antigenic sites on the N protein were able to decrease nucleocapsid accumulation and the release of infectious virus. The MAbs describing the two antigenic sites on NS protein also had an antiviral effect on ERA virus. When an anti-N MAb (0.5 ng per cell) was introduced into CVS-infected cells, virus inhibition was complete if the anti-N MAb was introduced between 0 and 5 h post-infection and ineffective beyond 9 h post-infection. The inhibition was dose-dependent. The MAbs could block virus multiplication either by 'neutralizing' newly translated N and NS proteins or by impairing the initial transcription of the genome.
J Gen Virol 1987 Dec
PMID:Antiviral activity of monoclonal antibodies specific for the internal proteins N and NS of rabies virus. 244 23


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