Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of external pH on the amplitude of currents through single sodium channels in cultured mouse neuroblastoma cells C 1300, clone N18A-1 was studied. Currents through single sodium channels in outside-out membrane patches were measured at normal (7.2) and low (5.4) pH of the external solution. With a decrease of the external pH to 5.4, about two-fold reversible reduction of the amplitude of single sodium channel currents (at testing potentials of -10-30 mV) was observed. The data obtained confirm the suggestion that the inhibition of macroscopic sodium currents with lowering of pH of the extracellular solution is due to the decrease in the ionic current flowing through single open channels.
 ...
PMID:[Hydrogen ion block of single sodium channels in neuroblastoma cells]. 254 14

The effects of temperature on the properties of sodium channels from mouse neuroblastoma cells modified by the pyrethroid insecticide deltamethrin were investigated using the patch-clamp technique. The study was aimed at determining various states of modified channels which were expected to be revealed by raising the temperature as a result of an increase in channel activity. After exposure to 10 microM deltamethrin, the decay of whole cell sodium current at -30 mV was drastically slowed. It is expressed by two exponential functions at 11 degrees C and by three exponential functions at room temperature (22 +/- 1 degree C). Thus, raising the temperature reveals a new process. Whole cell sodium tail currents associated with step repolarization from -30 mV to -100 mV were best fit by the sum of two exponential functions both at 11 degrees C and at room temperature. The decay of the summed modified single sodium channel currents at -30 mV was expressed by a single exponential function at 11 degrees C, and by two exponential functions at room temperature. In keeping with these results, the open time histograms show the single (11 degrees C) and double (room temperature) exponential distributions. Thus, raising the temperature allows a new single channel process to be revealed. Other modified open states observed previously at 11 degrees C were also found at room temperature including a flickering state and a subconducting state. In addition, several new subconducting states were found at room temperature.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Temperature-dependent subconducting states and kinetics of deltamethrin-modified sodium channels of neuroblastoma cells. 254 81

Patch clamp studies of neuroblastoma cells have shown that in the presence of sodium hydrogen sulfide (NaHS; the in vitro precursor of H2S), addition of the sulfonated amino acids, taurine or cysteic acid resulted in reversible abolition of the inward sodium currents. This effect could also be demonstrated by preincubating cells for 3-20 min with 5-10 mM NaHS followed by replacement of the solution with taurine or cysteic acid in sulfide-free saline. Neither NaHS, taurine nor cysteic acid alone had any effect. The sulfhydryl reagents, beta-mercaptoethanol and dithiothreitol, were also found to abolish reversibly the sodium currents. As the effects of the above treatments were nearly identical, the synergistic action of NaHS with taurine or cysteic acid may result from reduction of the disulfide bonds between subunits comprising the sodium channel. The responses to NaHS and taurine, a putative neurotransmitter/neuromodulator, suggest that reductions in sodium channel function may be the mechanism(s) responsible for loss of central respiratory drive during H2S poisoning.
 ...
PMID:Hydrogen sulfide in combination with taurine or cysteic acid reversibly abolishes sodium currents in neuroblastoma cells. 255 75

We have studied the behaviour of single sodium channels in cell-attached patches in neuroblastoma cell line N1E 115 at 8-15 degrees C modified by chloramine-T (CT). Application of the agent to the external surface of the membrane cause different effects: CT binds to the membrane and cause irreversible effects leading to a decrease of open channel lifetime at 10 or 20 mV relative potentials without affecting the amplitude of single channel current. Channels modified by CT show a tendency to occur in burst (they can open and close several times during depolarization). Therefore, the slower decay of the average current must be explained by the flickering behaviour of the modified channels. We also examined the effect of CT on the relationship between open time of the channels and membrane potential. On the other hand, a small decrease in the mean delay time as a function of membrane voltages was observed which probably is related to the three state model of inactivation. Our results suggest that CT modifies sodium channel inactivation.
 ...
PMID:Modification of single sodium channels in neuroblastoma cells by chloramine-T. 256 85

We have investigated the effect of pharmacological agents on [14C]guanidinium ion influx through sodium channels in C6 rat glioma and N18 mouse neuroblastoma cells. The sodium channels of the N18 cells can be activated by aconitine alone, indicating that they are voltage-dependent channels. In contrast, sodium channels in the C6 cells require the synergistic action of aconitine and scorpion toxin for activation and are therefore characterized as so-called silent channels. The general anesthetic halothane used at clinical concentrations, specifically inhibited the ion flux through the silent sodium channel of C6 rat glioma cells. The voltage-dependent channels of the N18 cells were insensitive to halothane at the concentrations tested.
 ...
PMID:Halothane inhibits the neurotoxin stimulated [14C]guanidinium influx through 'silent' sodium channels in rat glioma C6 cells. 257 48

The actions of diphenylhydantoin (DPH) and carbamazepine (CBZ) on sodium channels in mouse neuroblastoma cells (clone N18) were analyzed using the patch voltage clamp procedure in the whole cell configuration. DPH and CBZ reduced sodium currents without effect on the voltage dependence of sodium channel activation. Half-maximal inhibition was observed with approximately 30 microM of each drug. Depolarization increased and hyperpolarization reversed channel block by these two drugs in the voltage range from -90 to -45 mV. Repetitive stimulation at 2 Hz or greater enhanced inhibition of sodium channels. The half-time for recovery from voltage-dependent inhibition was greater for DPH (1.36 sec) than for CBZ (0.38 sec). A combination of prolonged depolarizing pulses of 15 mV with superimposed brief maximal depolarizations designed to mimic the electrical activity in an epileptic focus gave additive effects of voltage-dependent and frequency-dependent inhibition. The results support the previous proposal that DPH and CBZ are sodium channel-selective anticonvulsants and provide a potential basis for specific inhibition of neurons in epileptic foci. The mechanism of DPH and CBZ action is considered in terms of an allosteric or modulated receptor model of drug binding and action.
 ...
PMID:Voltage clamp analysis of the inhibitory actions of diphenylhydantoin and carbamazepine on voltage-sensitive sodium channels in neuroblastoma cells. 258 Nov 24

Measurement of neurotoxin binding in rat brain membranes and neurotoxin-activated 22Na+ influx in neuroblastoma cells were used to define the site and mechanism of action of pyrethroids and DDT on sodium channels. A highly potent pyrethroid, RU 39568, alone enhanced the binding of [3H]batrachotoxinin A 20-alpha-benzoate up to 30 times. This effect was amplified by the action of neurotoxins such as sea anemone toxins and brevetoxin acting at different sites of the sodium channel protein in brain membranes. The ability of various pyrethroids and DDT to enhance batrachotoxin binding was related to their capacity to activate tetrodotoxin sensitive 22Na+ uptake. These results point to an allosteric mechanism of pyrethroids and DDT action involving preferential binding to active states of sodium channels which have high affinity for neurotoxins, causing persistent activation of sodium channels. Pyrethroids do not block [3H]tetrodotoxin binding, 125I-Anemonia sulcata toxin 2 binding, 125I-Tityus serrulatus toxin gamma binding at neurotoxin receptor sites 1, 3 and 4 respectively. Pyrethroids appear to act at a new neurotoxin receptor site on the sodium channel. The distribution of pyrethroid binding sites in rat brain was determined by quantitative autoradiographic procedures using the property of pyrethroids to reveal binding sites for [3H]batrachotoxinin A 20-alpha-benzoate.
 ...
PMID:Interaction of insecticides of the pyrethroid family with specific binding sites on the voltage-dependent sodium channel from mammalian brain. 284 61

Blood plasma, serum and its fractions containing components of different molecular masses obtained by dialysis and gradual ultrafiltration were tested for their action on the sodium currents of voltage clamped internally perfused neuroblastoma cells. Blood plasma free of platelet factor 4, serum and its fractions containing components of molecular masses more than 50 kD produced an increase in sodium channel currents and shifts in activation and inactivation curves along the voltage axis towards more negative or positive potentials, respectively. Moreover, the serum deficient in components with the molecular masses less than 50 kD produced a more prominent effect on all the parameters tested. Thus, the low-molecular fractions were suggested to exert an inhibitory activity on the stimulatory effects produced by the high-molecular components of the serum.
 ...
PMID:[Effect of blood plasma and serum and its fractions on the activity of the sodium channels in neuroblastoma cells]. 285 74

In the presence of ouabain, veratridine enhances sodium influx in the mouse neuroblastoma cell line Neuro-2A (ATCC, CCL131), causing cellular swelling and subsequent death. Tetrodotoxin (puffer fish toxin) or saxitoxin (paralytic shellfish poison), both of which block the sodium channel of excitable membranes, antagonize this effect, enabling cell growth to continue. This phenomenon was used as the basis of a new assay for these toxins. It is also possible to estimate the quantity of TTX from the relationship between TTX concentration and percentage of living cells. This new method is simple, inexpensive, and sensitive, and may replace the conventional mouse bioassay.
 ...
PMID:A tissue culture assay for tetrodotoxin, saxitoxin and related toxins. 336 66

Sodium currents mediated by voltage-sensitive sodium channels in normal and scorpion toxin-resistant neuroblastoma cells were measured using a giga-ohm seal recording method in the whole cell patch configuration. The voltage and time dependence of sodium currents were similar in normal and mutant cell lines. Half-maximal activation occurred for test depolarizations in the range of -7 to -11 mV. Half-maximal inactivation occurred for pre-pulses in the range of -62 to -69 mV. Scorpion toxin from Leiurus quinquestriatus (100 to 200 nM) increased the time constant for sodium channel inactivation 6- to 9-fold, increased the peak sodium current 2.0 +/- 0.5-fold, shifted the voltage dependence of sodium channel activation 7 to 11 mV to more negative potentials, and made the voltage dependence of inactivation less steep. These effects were observed for both normal and scorpion toxin-resistant neuroblastoma cells. However, the effect of Leiurus toxin on the rate of inactivation was half-maximal at 1.7 nM for the parental cell line N18, in contrast to 5.4 or 39 nM for the scorpion toxin-resistant clone LV30 and 24 or 51 nM for LV10. These results show that scorpion toxin resistance results from a specific change in channel properties that does not impair normal function but causes an increase in the apparent KD for Leiurus toxin action on sodium channels.
 ...
PMID:Voltage clamp analysis of sodium channels in normal and scorpion toxin-resistant neuroblastoma cells. 609 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>