Differentiation of NG108-15 cells induced by the combined presence of dbcAMP and dexamethasone brings about the expression of N and P/Q types of calcium channels and the inhibitory influence of muscarinic receptors on calcium influx
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
11489263
DOI
10.1016/s0006-8993(01)02701-9
PII: S0006-8993(01)02701-9
Knihovny.cz E-resources
- MeSH
- Muscarinic Antagonists pharmacology MeSH
- Calcium Channel Blockers pharmacology MeSH
- Cell Differentiation drug effects physiology MeSH
- Cholinergic Agonists pharmacology MeSH
- Dexamethasone pharmacology MeSH
- Bucladesine pharmacology MeSH
- Intracellular Fluid drug effects metabolism MeSH
- Carbachol pharmacology MeSH
- Cells, Cultured drug effects metabolism MeSH
- Drug Interactions physiology MeSH
- Humans MeSH
- Membrane Potentials drug effects physiology MeSH
- Nifedipine pharmacology MeSH
- Receptors, Muscarinic drug effects metabolism MeSH
- Gene Expression Regulation drug effects physiology MeSH
- Tretinoin pharmacology MeSH
- Calcium metabolism MeSH
- Calcium Signaling drug effects physiology MeSH
- Calcium Channels, N-Type drug effects metabolism MeSH
- Calcium Channels, P-Type drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Muscarinic Antagonists MeSH
- Calcium Channel Blockers MeSH
- Cholinergic Agonists MeSH
- Dexamethasone MeSH
- Bucladesine MeSH
- Carbachol MeSH
- Nifedipine MeSH
- Receptors, Muscarinic MeSH
- Tretinoin MeSH
- Calcium MeSH
- Calcium Channels, N-Type MeSH
- Calcium Channels, P-Type MeSH
Differentiation of cholinergic cell line NG108-15 induced by a combination of dibutyryl cyclic AMP (dbcAMP) and dexamethasone enhances the cholinergic phenotype of the cells more than that induced by either agent alone. We investigated the effect of treatment with dbcAMP and dexamethasone on potassium depolarization-evoked influx of calcium and its regulation by the muscarinic agonist carbachol. Depolarization of control cells and of cells differentiated in the presence of dbcAMP or dexamethasone alone, or in the combined presence of dbcAMP and dexamethasone induced, respectively, 2.2-, 4.3-, 2.7- and 10.7-fold increases of the resting [Ca(2+)](i). Dexamethasone alone and the combination of dbcAMP and dexamethasone augmented the number of muscarinic receptors by 25 and 40%, respectively. Inhibitors of N (omega-conotoxin GVIA) or P/Q (omega-agatoxin TK) calcium channels had no effect on Ca(2+) influx in control cells, whereas in cells differentiated in the combined presence of dbcAMP and dexamethasone they significantly diminished the influx of Ca(2+) by 20 and 5%, respectively. Carbachol attenuated calcium influx in differentiated cells in an atropine-insensitive manner if it was present during stimulation. This effect of carbachol was probably due to an open-channel block of L type channels. In the presence of nifedipine, carbachol attenuated the influx of Ca(2+) into cells differentiated with dbcAMP and dexamethasone by 20% in an atropine-sensitive way. Data show that differentiation of NG108-15 cells by dbcAMP and dexamethasone promotes the expression of functional nifedipine-insensitive N and P/Q types of Ca(2+) channels and that the nifedipine-insensitive calcium influx becomes subject to inhibitory regulation by muscarinic receptors.
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