Effects of drug‐induced paralysis and depolarisation on acetylcholine receptor and cyclic nucleotide levels of chick muscle cultures

Betz, Heinrich

doi:10.1016/0014-5793(80)80240-7

Cited by 8 publications

(2 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cultured myotubes exhibit spontaneous, intermittent electromechanical activity, and it is well established that treatments that block or stimulate this activity (and thereby reduce or enhance the average level of cytosolic calcium) lead to a stimulation or reduction, respectively, of the AcChR synthesis rate (Cohen and Fischbach, 1973;Shainberg and Burstein, 1976;Betz, 1980). Calcium ions are obvious candidates for second messenger in this signaling pathway, and the question arises as to whether they bind to calmodulin, a protein that mediates regulatory effects of calcium in many other cells, to shut off receptor synthesis.…”

Section: Discussionmentioning

confidence: 99%

Trifluoperazine Stimulates Acetylcholine Receptor Synthesis in Cultured Chick Myotubes

Schneider

Shieh

Pezzementi

et al. 1984

Journal of Neurochemistry

View full text Add to dashboard Cite

Acetylcholine receptor appearance rate in the presence of the phenothiazines trifluoperazine and chlorpromazine was measured in cultured embryonic chick myotubes by means of 125I-alpha-bungarotoxin. At drug concentrations of 5 to 10 X 10(-6) M, receptor appearance rate was significantly enhanced while receptor half-life, cellular protein, net protein synthesis rate, and acetylcholinesterase levels were not similarly affected. The sulfoxide derivatives were without effect. At concentrations of 3 X 10(-5) M and above, both trifluoperazine and chlorpromazine caused myotube contracture and cell loss. Drug combination experiments revealed that receptor stimulation caused by phenothiazines is overcome by low concentrations of veratridine and ryanodine, but not by membrane depolarization with 20 mM KCl. These results lend support to the role of calcium as an intracellular messenger in acetylcholine receptor synthesis regulation, but are difficult to reconcile with the notion that cytosolic calmodulin serves as the calcium receptor in this signaling pathway. Since the trifluoperazine effect resembles that caused by the calcium antagonist D-600, phenothiazines may stimulate receptor synthesis by blocking a voltage-gated calcium channel.

show abstract

Section: Discussionmentioning

confidence: 99%

Trifluoperazine Stimulates Acetylcholine Receptor Synthesis in Cultured Chick Myotubes

Schneider

Shieh

Pezzementi

et al. 1984

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…1977). Addition of tetrodotoxin or D-600 (an antagonist of voltage-sensitive Ca2+ channels) to these spontaneously active cells produces an increase in nAChR number (Betz, 1980;Shieh et al, 1983). Addition of A23 187, a Ca2+ ionophore, to cultured rat diaphragm blocked the increase in receptor number associated with denervation in culture (Forrest et al, 1981), a finding suggesting that changes in cytosolic Ca2+ level may mediate the alteration in nAChR synthesis produced by changes in receptor activation.…”

mentioning

confidence: 99%

Effects of Prolonged Depolarization on the Nicotinic Acetylcholine Receptors of PC12 Cells

DeLorme

McGee

1988

Journal of Neurochemistry

View full text Add to dashboard Cite

To determine whether prolonged depolarization and/or changes in intracellular Ca2+ concentrations stimulate adaptive responses of neuronal nicotinic acetylcholine receptors, PC12 pheochromocytoma cells were grown in medium containing various concentrations of K+. Nicotinic receptor function was determined as carbachol-stimulated uptake of 86Rb+. Cells were exposed to 50 mM K+ for up to 4 days and then allowed to repolarize for 60 min. Under these conditions, no changes in basal or carbachol-stimulated uptake of 86Rb+ were observed. Furthermore, neither the time course of carbachol-stimulated uptake or the carbachol concentration dependence of 86Rb+ uptake was altered. Finally, concurrent depolarization did not affect the functional down-regulation produced by chronic exposure of the cells to carbachol. Thus, neuronal nicotinic acetylcholine receptors on PC12 cells do not appear to be regulated by depolarization or prolonged elevation of the intracellular Ca2+ level.

show abstract

The Acetylcholine Receptor: Control of Its Synthesis, Stability, and Cell Surface Distribution

Betz

1981

Proceedings in Life Sciences

View full text Add to dashboard Cite

Effects of drug‐induced paralysis and depolarisation on acetylcholine receptor and cyclic nucleotide levels of chick muscle cultures

Cited by 8 publications

References 28 publications

Trifluoperazine Stimulates Acetylcholine Receptor Synthesis in Cultured Chick Myotubes

Trifluoperazine Stimulates Acetylcholine Receptor Synthesis in Cultured Chick Myotubes

Effects of Prolonged Depolarization on the Nicotinic Acetylcholine Receptors of PC12 Cells

The Acetylcholine Receptor: Control of Its Synthesis, Stability, and Cell Surface Distribution

Contact Info

Product

Resources

About