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)

Outward currents were recorded from voltage-clamped NG108-15 mouse neuroblastoma X rat glioma hybrid cells, differentiated with prostaglandin E1. Depolarising voltage steps from -70 mV, evoked a transient outward current from a threshold of -30 mV. The outward current showed complete inactivation at potentials positive to -10 mV. Inactivation was removed by hyperpolarisation with half-inactivation at -53 mV. The time course of the inactivation could be best fitted by two exponentials with mean time constants of 280 ms and 1.6 s at +80 mV. Tail current measurements showed a shift in the reversal potential with changes in external K+ concentration, consistent with K+ as the current-carrying ion. The outward current amplitude was reversibly reduced by 4-aminopyridine, and the time course of inactivation modified. In the presence of other K+ channel blockers (tetraethylammonium, barium and tetrahydroaminoacridine) the amplitude of the outward current was also reversibly reduced, but with a negligible effect on its time course. The current was unaffected by dendrotoxin, d-tubocurarine, apamin, Cd2+ and Ni2+, and by replacing external Ca2+ with Co2+ or Mg2+. In current clamp, action potential duration was greatly increased by 4-aminopyridine. The findings show that the NG108-15 cell line displays a transient outward current that resembles IK(A) but with a higher than usual threshold and relatively slow inactivation, and that this current is likely to be important for action potential repolarisation.
 ...
PMID:A transient outward current in NG108-15 neuroblastoma x glioma hybrid cells. 235 30

1. Two types of voltage-sensitive calcium channels were identified and studied in the neuroblastoma cell line N1E-115. Calcium channel currents as carried by Ba2+ (50 mM) were recorded using the whole-cell variation of the patch-electrode voltage-clamp technique. 2. A transient (type I) inward Ba2+ current was evoked by a step depolarization from a holding potential of -80 mV to potentials more positive than -50 mV. The current amplitude became maximum around -20 mV. 3. A depolarization to potentials more positive than -20 mV evoked a long-lasting (type II) component of the inward Ba2+ current. This component reached its maximum around +10 mV and did not inactivate during a prolonged depolarizing pulse lasting 400 ms. 4. When preceded by a 5 s conditioning pulse to -30 mV, step depolarization failed to evoke a transient current due to inactivation. However, it induced a long-lasting current. 5. A transient current isolated as the component sensitive to conditioning depolarization became faster in its time course and smaller in its amplitude with membrane depolarization. The current direction was still inward at +60 mV. 6. From the differential voltage sensitivity and the independent channel activity described above, calcium channels responsible for the transient current (type I channel) and those responsible for the long-lasting current (type II channel) were considered to be two different entities. 7. Cd2+ preferentially blocked type II channels, whereas La3+ was a highly potent blocker for both types of calcium channels. 8. The relative potency for block by polyvalent cations was as follows (apparent dissociation constant in microM): La3+, 1.5 much greater than Ni2+, 47 greater than Cd2+, 160 = Co2+, 160 for type I channels, and La3+, 0.9 greater than Cd2+, 7.0 much greater than Ni2+, 280 greater than Co2+, 560 for type II channels. 9. The two types of calcium channels were equally sensitive to the temperature. The current amplitude was reduced by cooling below 30 degrees C. The temperature coefficient (Q10) value was estimated to be 3.0 between 20 and 30 degrees C, and 15.0 below 20 degrees C. Above 30 degrees C, warming reduced the amplitude slightly. 10. External application of dibutyryl adenosine 3',5'-phosphate (dibutyryl cyclic AMP) (1 mM) caused an increase in the amplitude of the type II current by 30-50%, while failing to enhance the type I component.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Characterization of two types of calcium channels in mouse neuroblastoma cells. 244 46

Cd2+ and other divalent metals mobilized cell Ca2+ in human skin fibroblasts. The divalent metals produced a large spike in cytosolic free Ca2+ and strikingly increased net Ca2+ efflux similarly to bradykinin. One-tenth microM Cd2+ half-maximally increased 45Ca2+ efflux. The potency order of the Ca2+ mobilizing metals was: Cd2+ greater than Co2+ greater than Ni2+ greater than Fe2+ greater than Mn2+. Cd2+ probably acts at an extracellular site because loading the cells with a heavy metal chelator only slightly inhibited Cd2+-evoked 45Ca2+ efflux. Cd2+ increased [3H]inositol polyphosphates; [3H]inositol trisphosphate increased 4-fold in 15 s. Zn2+ reversibly blocked 45Ca2+ efflux evoked by Cd2+ but not that produced by bradykinin. Zn2+ competitively (Ki = approximately 0.4 microM) inhibited net Ca2+ efflux produced by Cd2+. Cd2+ also evoked Ca2+ mobilization in umbilical artery muscle, endothelial, and neuroblastoma cells, and the divalent cation agonist and antagonist specificities were similar to those in the fibroblasts. The divalent metals appear to trigger Ca2+ mobilization via a reversible interaction with an external site on the cell surface, which may be considered a "Cd2+ receptor."
 ...
PMID:Cadmium evokes inositol polyphosphate formation and calcium mobilization. Evidence for a cell surface receptor that cadmium stimulates and zinc antagonizes. 254 Jan 74

The action of several ligands on the low- (LVA,T) and high-threshold (HVA,L and N) Ca channels of adult rat sensory neurons and human neuroblastoma IMR32 cells has been investigated. In both cell types, 40 microM Cd2+ and 6.4 microM /omega-Conotoxin (omega-CgTx) selectively blocked the HVA channels, sparing the majority of LVA channels that were antagonized by amiloride and Ni2+. In 50% of the cells, however, /omega-CgTx spared also a 15% of HVA channels that proved to be sensitive to BAY K 8644. The agonistic action of BAY K 8644 on [omega-CgTx-resistant HVA channels caused a large Ba current increase, prolonged current deactivation and acceleration of HVA channels inactivation that was particularly evident in adult rat DRG.
 ...
PMID:Action of Ca2+ agonists/antagonists in mammalian peripheral neurons. 256 66

The mechanisms of action of two different serotonin receptors, found in a neuronal cell line (neuroblastoma X glioma hybrid cells) and in a non-excitable glioma cell line, were explored. In both cell lines, serotonin induced a dose-dependent, transient rise of cytosolic Ca2+ activity (measured by fura-2 or indo-1 fluorescence). Ca2+ channel blockers (Ni2+ and La3+, not nifedipine) suppressed the Ca2+ response to serotonin in the hybrid cells but not in the glioma cells. After application of Ca2+ ionophores (ionomycin and A23187) in order to short-circuit internal Ca2+ stores, serotonin was still able to induce a Ca2+ response in the hybrid cells but not in the glioma cells. Serotonin dose-dependently stimulated the rate of 45Ca2+ uptake several-fold in the hybrid cells, but hardly at all in the glioma cells. Thus, in the neuronal cell line cytosolic Ca2+ activity is raised through enhancement of Ca2+ entry into the cells from the extracellular environment via 5-HT3 receptors (blocked by ICS 205-930, MDL 72222 and GR 38032 F). The depolarization response caused by serotonin in the hybrid cells is due to activation of cation conductance(s), obviously allowing entry of extracellular Ca2+. In contrast to the neuronal cell line, in the glial cell line the rise of Ca2+ activity is mediated by ketanserin-susceptible 5-HT2 receptors (not affected by treatment with pertussis toxin) mainly liberating Ca2+ from internal stores. In the glioma cells the release of Ca2+ from internal stores leads to opening of Ca2+-dependent K+ channels, responsible for the hyperpolarizing response. Thus, the neuronal and the glial cell lines might provide suitable systems in which to study the diverse cellular functions triggered by the rise of cytosolic Ca2+ activity, which is caused by different serotonin receptors.
 ...
PMID:Serotonin regulates cytosolic Ca2+ activity and membrane potential in a neuronal and in a glial cell line via 5-HT3 and 5-HT2 receptors by different mechanisms. 260 42

Quantification of nickel in animal soft tissue is of toxicological interest. A digestion method applying the use of microwave ovens for irradiating samples in Teflon digesters was developed. An acid mixture containing nitric acid (16 M, 1.0 ml g-1 tissue), hydrochloric acid (6 M, 0.5 ml g-1 tissue) and H2O2 (30%, 1.0 ml g-1 tissue) and irradiation at 600 W for 5 min were required for complete dissolution of tissue matrices and nickel compounds. Analyses of Ni in National Bureau of Standards Reference Material 1566 oyster tissue gave 0.87 +/- 0.24 micrograms g 1(mean +/- SD, n = 5), which was in agreement with the NBS certified value of 1.03 +/- 0.19 micrograms g-1. Recoveries of 1-300 micrograms Ni added as nickel sulfate (highly soluble), nickel subsulfide (moderately soluble in biological fluids and acid) or nickel oxide (green high-temperature oxide, low solubility in biological fluids and acid) to lung, liver, lymph node and kidney were quantitative, except in the case of nickel sulfate added to kidney, where recovery was less than quantitative for 1-10 micrograms Ni. The method appears effective for digestion of a variety of tissues requiring Ni analyses.
 ...
PMID:A rapid digestion method for analysis of nickel compounds in tissue by electrothermal atomic absorption spectrometry. 277 54

A method for the determination of selenium in human spermatozoa and prostasomes is described. The samples were digested with 25% (w/v) tetramethylammonium hydroxide (TMAH) in methanol and analyzed by atomic absorption spectrometry with electrothermal atomization and Zeeman background correction (ET-AAS). Nickel was used as a matrix modifier. Calibration was performed using the matrix-based calibration curve. The TMAH-digestion method agreed well with a conventional digestion procedure using concentrated nitric acid. The TMAH-digestion does not require heating or strong acids and it was suitable for small biological samples. The average recovery of added selenium in spermatozoan digests was 95.1 +/- 5.2% (n = 5). The coefficient of variation was 9.1% (n = 21). The accuracy of the method tested with the NBS standard 1577 (bovine liver, certified at 1.1 +/- 0.1 micrograms Se/g) resulted in a value of 0.98 +/- 0.10 micrograms Se/g (n = 16). The method was further tested in an interlaboratory comparison study.
 ...
PMID:Determination of selenium in human spermatozoa and prostasomes using base digestion and electrothermal atomic absorption spectrophotometry. 367 30

Twenty common toxic chemicals were tested for their ability to inhibit respiratory activity in cultured mouse neuroblastoma C1300 cells, clone 41A3. Pentachlorophenol and hexachlorophene exhibited the properties of uncouplers of oxidative phosphorylation, whereas for KCN, pyridine, 2,5-hexandione, NaAsO2, K2Cr2O7, HgCl2, methylmercury and triethyltin more simple time-courses of inhibition were obtained. Ethanol, methanol, dimethyl sulphoxide, benzidine, nickel acetate, MnCl2, phenol, CoCl2, Na2SeO3 and CdCl2 did not cause any significant changes in respiratory activity. Among the effective compounds, those with well-known neurotoxic properties were the most potent in inhibiting respiration in 41A3 cells.
 ...
PMID:Effects of toxic chemicals on the respiratory activity of cultured mouse neuroblastoma cells. 407 60

The voltage-dependent Na+ ionophore of various neuronal cells is permeable not only to Na+ ions but also to guanidinium ions. Therefore, the veratridine- (or aconitine-)stimulated influx of [14C]guanidinium in neuroblastoma x glioma hybrid cells was measured to characterize the Na+ ionophore of these cells. Half-maximal stimulation of guanidinium uptake was seen at 30 microM veratridine. At 1 mM guanidinium, the veratridine-stimulated uptake of guanidinium was lowered to 50% by approximately 60 mM Li+, Na+, or K+ and by a few millimolar Mn2+, Co2+, or Ni2+. The basal, as well as the veratridine-stimulated, uptake of guanidinium was inhibited by the cholinergic antagonists (+)-tubocurarine (Ki = 50 to 500 nM) and atropine (Ki = 5 to 30 microM) and the adrenergic antagonists phentolamine (Ki = 5 microM) and propranolol (Ki = 60 microM). The specificity of the inhibitory effects of these agents is stressed by the ineffectiveness of various other neurotransmitter antagonists. However, the corresponding ionophore in neuroblastoma cells (clone N1E-115) seems to be regulated differently. While phentolamine and propranolol inhibit the veratridine-activated uptake as in the hybrid cells, (+)-tubocurarine and atropine exert only a slight effect.
 ...
PMID:Blockade by neurotransmitter antagonists of veratridine-activated ion channels in neuronal cell lines. 613 Jan 27

Several calcium antagonists were screened for their effect on muscarinic acetylcholine receptor-mediated cyclic GMP formation in murine neuroblastoma cells (clone N1E-115). Mn2+, Ni2+, and verapamil rapidly antagonized the response noncompetitively, with the following order of potency: verapamil greater than Mn2+ greater than Ni2+. The effects of Mn2+ and Ni2+, but not those of verapamil, were largely reversed by increasing extracellular calcium concentration. Additional effects of these agents included displacement of [3H]quinuclidinyl benzilate binding by verapamil and elevation of cyclic GMP levels by Mn2+ and Ni2+ in the absence of agonists. These results are in support of the hypothesis that receptor-mediated cyclic GMP formation by these cells is dependent upon entry of calcium into the cell and demonstrate the complexity of the effects of calcium antagonists.
 ...
PMID:Effect of some calcium antagonists on muscarinic receptor-mediated cyclic GMP formation. 629 67


<< Previous 1 2 3 4 5 6 7 Next >>