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)

When SK-N-SH human neuroblastoma cells were exposed to nicotine (NIC) or KCl they showed a dose-dependent transient increase (2- to 4-fold) in intracellular Ca2+ concentration ([Ca2+])i as detected by quin-2 fluorescence, with half maximal effects (EC50) observed at 13 microM and 26 mM, respectively. Tubocurarine and 1-isodihydrohistrionicotoxin potently blocked the NIC-evoked (IC50 congruent to 1 microM and 0.3 microM, respectively), but not the high [K+]o-evoked [Ca2+]i accumulation. The KCl-induced response was inhibited by verapamil and diltiazem (IC50 = 1.4 and 10.9 microM, respectively). Tetrodotoxin (3 microM) and tetraethylammonium (10 microM) had no effect on [Ca2+]i accumulation induced by either agent. Increases in [Ca2+]i could be evoked sequentially by NIC and KCl in the same cells suggesting independent mechanisms of Ca2+ entry. In a Ca2+-free medium, no response to either KCl or NIC was observed. However, when Ca2+ ions were restored, [Ca2+]i accumulation was enhanced to the same extent as cells suspended in a Ca2+-containing buffer. Long-term (18 hr) pretreatment of SK-N-SH cells with pertussis (100 ng/ml) or cholera toxins (10 nM) had no effect on NIC or KCl-induced [Ca2+]i accumulation. Together, these data demonstrate the presence of NIC receptors and voltage-sensitive Ca2+ channels on SK-N-SH neuroblastoma cells, through which [Ca2+]i may be modulated.
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PMID:Calcium influx mediated by nicotinic receptors and voltage sensitive calcium channels in SK-N-SH human neuroblastoma cells. 254 92

Substance P stimulated the uptake of guanidinium in neuroblastoma X glioma hybrid cells and neuroblastoma cells but not in polyploid glioma cells. Guanidinium has previously been shown to pass the action potential Na+ channel in the two neuronal cell lines. Half-maximal stimulation was reached at 3 microM substance P and, with the hybrid cells, a saturation was seen above 10 microM. The analogue (D-Pro2,D-Trp7,9)-substance P, recently described as a substance P antagonist, caused a stimulation of guanidinium uptake comparable to that seen in the presence of substance P and did not inhibit the stimulation exerted by substance P. The pharmacological properties of the substance P-activated ion channel were investigated. Tubocurarine, phentolamine and propranolol blocked the substance P-stimulated guanidinium uptake with half-maximal inhibitory concentrations of 0.5, 5 and 50 microM. A similar characteristics has been found previously with the veratridine-activated Na+ channel in the cell lines investigated here. Peptides structurally related to substance P such as physalaemin and eledoisin, or others such as neurotensin, bradykinin, D-Ala2, Met5-enkephalinamide and ACTH(1-24) did not affect guanidinium uptake. In view of the high concentrations of substance P required for eliciting an effect in the cell lines, the involvement of specific receptors is questioned. A direct interaction of the peptide with the action potential Na+ channel is discussed.
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PMID:Substance P enhances cation permeability of neuronal cell lines. 618 89

In SH-SY5Y human neuroblastoma cells, addition of acetylcholine or carbachol rapidly induces a transient protrusion of lamellipodia. The protrusions appear after a delay of 30 sec and persist for a period of about 5 min at the margins of cell somata and at the distal parts of cell processes. They are caused by a strikingly increased, cytochalasin B-sensitive assembly of actin at the cell periphery. They often detach from the substrate, retracting and protruding again. In retinoic acid-induced neuronally differentiated cells, this initialized protrusive activity is restricted to growth cones. d-Tubocurarine does not influence, but atropine totally inhibits the cholinergic induction of the actin-driven protrusions, suggesting that a muscarinic receptor-mediated activation of the phosphoinositol signaling pathway is involved. Depolarization by increase of the potassium concentration and ionophore-mediated Ca(2+)-influx are ineffective to trigger the protrusive and ruffling activity. An identical cytochalasin B-sensitive actin-driven response is caused by treating of the cells with the protein kinase C (PKC) activator 12-myristate-13-acetate. In this case, however, lamellar protrusions are formed after a delay of at least 3 min and are maintained for several days. Incubating the cells with the protein kinase C inhibitor bisindolylmaleide or staurosporine inhibits both the muscarinic receptor-mediated and phorbolester-mediated actin-driven response, suggesting that activated PKC plays a crucial role.
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PMID:Muscarinic receptor-mediated induction of actin-driven lamellar protrusions in neuroblastoma cell somata and growth cones. Involvement of protein kinase C. 765 99