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

The cell line C9 used in this paper has a resting potential of --50 mV (+/- 10 mV) but is unable to generate an action potential upon electrical stimulation. The cell membrane has receptors for the selectivity filter toxin tetrodotoxin as well as for the gating system toxins, veratridine, scorpion toxin and sea anemone toxin. The Na+ channel which remains silent to electrical stimulation in the absence of toxins can be chemically activated by the gating system toxins. This has been demonstarted by electrophysiological techniques and by 22Na+ flux studies. The electrophysiological approach has shown that the sea anemone toxin is able to induce a spontaneous slow-wave activity inhibited by tetrodotoxin. 22Na+ influx analyses have shown that veratridine and the sea anemone toxin produce an important increase of the initial rate of 22Na+ influx into the C9 cell. The stimulation of 22Na+ entry by these gating system toxins is similar to that found using spiking neuroblastoma cells. Veratridine and the sea anemone toxin on one hand as well as veratridine and the scorpion toxin on the other hand are synergistic in their action to stabilize an open and highly permeable form of the sodium channel. Stimulation of 22Na+ entry into the cell through the sodium channel maintained open by the gating system neurotoxins is completely suppressed by tetrodotoxin.
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PMID:The sodium channel in non-impulsive cells. Interaction with specific neurotoxins. 4 40

Lithium ion entry at low concentrations (1 to 5 mM) into an electrically active adrenergic clone of mouse neuroblastoma cells was stimulated by veratridine; and this stimulation was blocked by tetrodotoxin, These data provide biochemical evidence that lithium ions enter by way of the sodium channel which may be a major pathway for entry of this ion into electrically active cells.
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PMID:Lithium ion entry through the sodium channel of cultured mouse neuroblastoma cells: a biochemical study. 86 Jan 26

A quantitative assay for sodium channel blocking toxins such as tetrodotoxin and saxitoxin has been developed for use with a microtitre plate reader. Mouse neuroblastoma cells, which die rapidly in the presence of ouabain and veratridine, were protected by tetrodotoxin; surviving cells were detected by their uptake of the vital dye Neutral red which was quantified with a microtitre plate reader at 540 nm. A sigmoidal dose response curve was obtained and tetrodotoxin concentrations were readily measured over the range 10 nM to 500 nM (3.2-160 ng/ml). With this method, sodium channel blocking toxins were detected directly, without processing or concentration, in culture supernates of several marine bacteria, including Shewanella alga, Alteromonas tetraodonis, Listonella (Vibrio) pelagia, V. alginolyticus, V. anguillarum and V. tubiashi. Culture supernates of Shewanella alga contained up to 510 ng/ml of sodium channel blocking toxin (using tetrodotoxin as a standard).
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PMID:A tissue culture assay for direct detection of sodium channel blocking toxins in bacterial culture supernates. 132 May 84

The alkaloid pumiliotoxin B (PTX-B) "activates" voltage-dependent sodium channels in synaptoneurosomes and neuroblastoma cells. It appears that PTX-B activates sodium channels by interacting with a site that is allosterically coupled to other sites on the sodium channel, namely two scorpion toxin sites and the brevetoxin site. In guinea pig cortical synaptoneurosomes, alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin induce a dose-dependent potentiation of PTX-B-induced 22Na+ influx. The synergism with beta-scorpion toxin differentiates PTX-B from the alkaloid veratridine, which induces an activation of sodium channels that is not affected by beta-scorpion toxin. PTX-B does not inhibit [3H]batrachotoxinin-A benzoate ([3H]BTX-B) binding to the alkaloid site on sodium channels. On the other hand, aconitine, which activates sodium channels and inhibits [3H]BTX-B binding, induces a 22Na+ influx that, like PTX-B-induced 22Na+ influx, is potentiated by alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin. Inhibition of [3H]BTX-B binding by aconitine is reduced in the presence of PTX-B. Both a type I pyrethroid (allethrin) and a type II pyrethroid (fenvalerate) inhibit PTX-B- and PTX-B/alpha-scorpion toxin-mediated 22Na+ influx. Allethrin and fenvalerate also inhibit aconitine-mediated 22Na+ flux but not BTX-mediated 22Na+ influx. It is proposed that on the sodium channel there is an "alkaloid-binding domain" at which alkaloids exert stimulatory actions. However, depending on the region on the domain to which the binding occurs, different allosteric interactions with other sites can be observed. PTX-B is proposed to interact with a part of the alkaloid-binding domain that is shared by aconitine but not by batrachotoxin or veratridine, whereas aconitine interacts with a part of the domain shared by PTX-B and by batrachotoxin/veratridine.
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PMID:Interaction of pumiliotoxin B with an "alkaloid-binding domain" on the voltage-dependent sodium channel. 133 16

Mouse monoclonal antibodies have been raised to the C-terminal region of rat type II voltage-dependent sodium channel. One of these, designated 13A4-G4, recognizes a 260 Kd putative sodium channel protein in human fetal brain, heart and skeletal muscle, at 14-18 weeks of gestation. Faint immunoreactivity is also present in human fetal kidney but none has been detected in human fetal liver, lung or spleen. The antibody reacts in both western blots and immunocytochemical preparations with the human neuroblastoma cell lines SK-N-SH and SK-N-MC, the rhabdomyoblastoma cell line TE671, Y79 retinoblastoma cells and IPSB-18 astrocytoma cells. No 13A4-G4 immunoreactivity has been detected in several human cell lines derived from tissues that do not normally express sodium channels.
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PMID:Immunochemical detection of sodium channel in human tissue and cell lines. 164 99

The effects of the lithium ion (Li+) on receptor-mediated synthesis of second messengers were determined, when cellular sodium channels were quiescent or excited, using the murine neuroblastoma clone (N1E-115). In this clone, lithium inhibited the receptor-mediated synthesis of cyclic AMP and cyclic GMP and it also increased the accumulation of inositol phosphates by a receptor-mediated process. When veratridine (20 microM) excited the sodium channel, the effects of lithium were potentiated. However, tetrodotoxin, a sodium channel blocker, completely prevented this potentiation. These results suggest that when neurons are depolarizing actively and intraneuronal levels of lithium increase by entry through the sodium channel, lithium has a more potent intracellular effect. As a result, lithium would have more potent and selective effects in those pathologically-active neurons underlying manic-depressive disorder.
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PMID:Potentiation by a sodium channel activator of effects of lithium ion on cyclic AMP, cyclic GMP and inositol phosphates. 165 Sep 29

A recent study of single sodium channel currents in neuroblastoma cells suggested interaction between ion channels in close proximity to one another (T. Kiss and K. Nagy, Eur. Biophys. J. 12, 13, 1985). The opening of one channel appeared to affect the likelihood that neighboring channels might open. Some of the conclusions were based on the analysis of observed channel openings that were segregated depending on whether one channel or more than one channel was open at the same time. We hypothesized that the longer one channel remained open, the more likely another channel operating independently, would open, thereby creating the impression of an apparent coupling of channel behavior. We performed simulations and measurements of single sodium channel currents to determine whether the technique of event segregation could account for apparent channel interactions. The simulations showed that the segregation of overlapping (more than one channel open at the same time) and nonoverlapping events led to a bias in the estimated open time and the derived closing rate. To avoid the bias, we found that random pairing of opening and closing events provided an unbiased estimate of the mean closing rate. Using this random assignment approach, we showed that the mean closing rate of single sodium channels in neonatal rat myocytes decreased with depolarization over a limited range of membrane potential. This suggested that the underlying closure mechanism(s) was voltage dependent. From the analysis of open times, we found no evidence for channel interaction in the time scale of tens of milliseconds. Depolarizing steps without events occurred in runs suggesting the existence of long-lived shut state(s). Double pulse experiments with the prepulse and test pulse above threshold showed significant inactivation of channels that did not open. The rate of inactivation of shut channels was substantially slower than the closure rate of open channels. The rate of inactivation of cardiac sodium channels appeared to be strongly dependent on the initial channel state.
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PMID:A source of bias in the analysis of single channel data: assessing the apparent interaction between channel proteins. 166 20

Blood plasma, serum and its fractions containing components of different molecular weights as well as some identified serum constituents were tested for their action on sodium currents of voltage-clamped, internally dialyzed neuroblastoma cells. Only components with a molecular weight over 50 kDa produced a persistent increase in sodium channel currents (stimulatory effect) and shifts in activation and inactivation curves along the voltage axis towards more negative or positive potentials, respectively (modifying effect). Both modulations taken together provide a somewhat higher level of sodium electro-excitable system activity. Among the identified serum components tested, including those possessing high physiological activity, albumin was the only one which reproduced the effects of whole blood serum both qualitatively and quantitatively. The data obtained allow to assume albumin to play a role of an active substance responsible for the blood plasma or serum effects on the potential-dependent transporting system in the neuroblastoma cell membrane. Albumin seems to be involved in holding the functional activity of sodium channels on a suitable level rather than being involved in any regulatory processes.
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PMID:The action of blood serum and its components on potential-dependent sodium channels in neuroblastoma cells. 166 55

Blood serum gamma-globulin and albumin were tested for their effect on the sodium currents of voltage clamped internally perfused serum deprived neuroblastoma cells. Albumin in the concentration corresponding to its content in 5% blood serum (22 microM) 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. These results both qualitatively and quantitatively reproduce the effects of 5% blood serum observed previously (Zubov, Sal'nikov, 1984, 1986). The addition of gamma-globulin failed to change the parameters registered. The data obtained led us to an assumption of the role of albumin as an active substance responsible for the effect of blood serum on the potential-dependent sodium-transporting system of neuroblastoma cell membrane.
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PMID:[The effect of the high-molecular components of the blood serum--gamma-globulin and albumin--on the sodium channel activity of neuroblastoma cells]. 170 91

Biochemical events leading to the formation of mature membrane-associated sodium channel proteins are not completely understood. We have recently purified a protein from the cytoplasm of brain cells, which is able to become incorporated into liposomes and induce neurotoxin-dependent sodium permeability. Here we report data on a monoclonal antibody derived against this protein. This antibody crossreacts with cell membrane preparations. The antibody binding to viable neuroblastoma cells is inhibited by veratrine, indicating that membrane molecules antigenically related to the cytoplasmic protein may also be related to the voltage-gated sodium channel.
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PMID:Possible relationship of brain cytoplasmic tetrodotoxin-sensitive protein to voltage-gated sodium channel shown by monoclonal antibody. 215 3


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