M1 muscarinic receptors mediate intracellular calcium release in NB-OK1 human neuroblastoma cells

1992 ◽  
Vol 346 (3) ◽  
Author(s):  
H.W.G.M. Boddeke ◽  
M. Buttini ◽  
M. Lichtsteiner ◽  
A. Enz
Keyword(s):  
Intracellular Calcium ◽  
Muscarinic Receptors ◽  
Calcium Release ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Intracellular Calcium Release ◽  
M1 Muscarinic ◽  
M1 Muscarinic Receptors

scholarly journals Adrenomedullin Stimulates Nitric Oxide Release from SK-N-SH Human Neuroblastoma Cells by Modulating Intracellular Calcium Mobilization

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2295-2305 ◽  
Author(s):  
Yong Xu ◽  
Teresa L. Krukoff
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Intracellular Calcium ◽  
Protein Kinase A ◽  
Neuroblastoma Cells ◽  
No Synthase ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
No Release ◽  
Kinase A

Abstract We used SK-N-SH human neuroblastoma cells to test the hypothesis that adrenomedullin (ADM), a multifunctional neuropeptide, stimulates nitric oxide (NO) release by modulating intracellular free calcium concentration ([Ca2+]i) in neuron-like cells. We used a nitrite assay to demonstrate that ADM (10 pm to 100 nm) stimulated NO release from the cells, with a maximal response observed with 1 nm at 30 min. This response was blocked by 1 nm ADM22–52, an ADM receptor antagonist or 2 μm vinyl-l-NIO, a neuronal NO synthase inhibitor. In addition, 5 μm 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester, an intracellular calcium chelator, eliminated the ADM-induced NO release. Similar results were observed when the cells were incubated in calcium-free medium or when l-type calcium channels were inhibited with 5 μm nifedipine or 10 μm nitrendipine. Depletion of calcium stores in the endoplasmic reticulum (ER) with 1 μm cyclopiazonic acid or 150 nm thapsigargin, or inhibition of ryanodine-sensitive receptors in the ER with 10 μm ryanodine attenuated the ADM-induced NO release. NO responses to ADM were mimicked by 1 mm dibutyryl cAMP, a cAMP analog, and were abrogated by 5 μm H-89, a protein kinase A inhibitor. Furthermore, Fluo-4 fluorescence-activated cell sorter analysis showed that ADM (1 nm) significantly increased [Ca2+]i at 30 min. This response was blocked by nifedipine (5 μm) or H-89 (5 μm) and was reduced by ryanodine (10 μm). These results suggest that ADM stimulates calcium influx through l-type calcium channels and ryanodine-sensitive calcium release from the ER, probably via cAMP-protein kinase A-dependent mechanisms. These elevations in [Ca2+]i cause activation of neuronal NO synthase and NO release.

scholarly journals Coupling of muscarinic receptors to the mobilization of intracellular Ca2+ stores in permeabilized SH-SY5Y human neuroblastoma cells

1990 ◽  
Vol 272 (1) ◽  
pp. 269-272 ◽  
Author(s):  
R J H Wojcikiewicz ◽  
S T Safrany ◽  
R A J Challiss ◽  
J Strupish ◽  
S R Nahorski
Keyword(s):  
Muscarinic Receptors ◽  
Neuroblastoma Cells ◽  
Dose Dependence ◽  
Maximal Response ◽  
Functional Coupling ◽  
Maximal Effect ◽  
Human Neuroblastoma Cells ◽  
Response Curves ◽  
Human Neuroblastoma ◽  
Intact Cells

Intracellular stores of Ca2+ were mobilized transiently by carbachol in suspensions of electrically permeabilized SH-SY5Y cells. The kinetics and the dose-dependence of this mobilization paralleled carbachol-induced increases in inositol 1,4,5-trisphosphate (InsP3) mass [for both parameters EC50 (concn. giving half-maximal response) = 60-70 microM]. Guanosine 5′-[gamma-thio]triphosphate enhanced the maximal effect and the potency of carbachol on Ca2+ mobilization and InsP3 mass, but caused separation of the dose-response curves (EC50 = 0.6 microM and 5.6 microM respectively). These data show that functional coupling of muscarinic receptors to Ca2+ mobilization can be maintained after permeabilization, reveal major effects of guanine nucleotides on agonist-induced Ca2+ mobilization and provide a basis for explanation of discrepancies between agonist potency on InsP3 concentration and Ca2+ mobilization in intact cells.

scholarly journals Crosstalk between VEGFR2 and muscarinic receptors regulates the mTOR pathway in serum starved SK-N-SH human neuroblastoma cells

2011 ◽  
Vol 23 (1) ◽  
pp. 239-248 ◽  
Author(s):  
Jacob Edelstein ◽  
Tianfeng Hao ◽  
Qin Cao ◽  
Leon Morales ◽  
Patricia Rockwell
Keyword(s):  
Muscarinic Receptors ◽  
Neuroblastoma Cells ◽  
Mtor Pathway ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma
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