Inhibitors of membrane depolarization regulate acetylcholine receptor synthesis by a calcium-dependent, cyclic nucleotide-independent mechanism

McManaman, James L.; Blosser, James C.; Appel, Stanley H.

doi:10.1016/0167-4889(82)90035-0

Cited by 28 publications

(7 citation statements)

References 14 publications

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“…Other recent studies have shown that A23187 treatment is able to mimic motor neuron innervation with regard to the regulation of enzymes involved in intermediary metabolism (31), maintenance of resting membrane potential (32), and acetylcholine receptor density (32,33). The effects on acetylcholine receptors are particularly relevant since receptor density is regulated by electrical activity both in vivo and in vitro (25).…”

Section: Discussionmentioning

confidence: 99%

Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

Sherman

Catterall

1984

Proc. Natl. Acad. Sci. U.S.A.

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Pharmacological blockade of the spontaneous electrical activity present in primary cultures of rat myotubes by growth in bupivacaine, tetrodotoxin, or KCI was found to increase the number of voltage-sensitive Na' channels 38-83% as measured by the specific binding of [3H]saxitoxin. The inhibition of spontaneous electrical activity and increase in channel density by bupivacaine displayed an identical dose response, with a half-maximal effect at 3.0 jiM. Growth of myotubes in the presence of 1 jIM A23187, a Ca2 -specific ionophore, resulted in a 30-60% decrease in the number of tetrodotoxin-sensitive channels with no change in affiity for [3H]saxitoxin. A23187 was able to overcome the increase in channel density produced by bupivacaine. These results suggest the presence of a Ca2+-mediated negative feedback system in which electrical excitability may be regulated by altering the number of tetrodotoxin-sensitive Na' channels.

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Section: Discussionmentioning

confidence: 99%

Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

Sherman

Catterall

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…There is reasonably good evidence that decreases in receptor number are associated with elevation of the intracellular Ca2+ level; substances like ryanodine and caffeine, which cause release of Ca2+ from the sarcoplasmic reticulum, decrease nAChR number (Shieh et al, 1983;Birnbaum et al, 1980). Thus, as expected, inhibitors of membrane depolarization, such as tetrodotoxin, produce increases in the number of nAChRs (Shieh et al, 1983), and these increases can be blocked by the calcium ionophore A23187 (McManaman et al, 1982;Rubin, 1985). These results suggest that nAChRs on muscle cells may be more subject to regulation by changes in electrical activity than are receptors on neuronal cells.…”

Section: Discussionmentioning

confidence: 93%

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

DeLorme

McGee

1988

Journal of Neurochemistry

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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.

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“…McManaman, and S. H. Appel, submitted). cAMP does not appear to be involved in the process by which muscle inactivity increases receptor number (McManaman et al, 1982). However, the presence of the P,-adrenergic receptor-linked adenylate cyclase system in skeletal muscle suggested that cAMP effects on ACh receptor synthesis may be under hormonal control.…”

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confidence: 97%

ß‐Adrenergic Receptor Activation Increases Acetylcholine Receptor Number in Cultured Skeletal Muscle Myotubes

Blosser¹

1983

Journal of Neurochemistry

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Treatment of embryonic chick muscle myotubes with the beta-adrenergic agonist isoproterenol increased the number of surface membrane nicotinic cholinergic receptors. Receptor degradation was unaffected by isoproterenol, suggesting that receptor synthesis was increased. The effect of isoproterenol appears to be mediated by the beta-adrenergic receptor adenylate cyclase system for the following reasons: (a) The response to isoproterenol was dose-dependent and stereospecific. (b) The response to catecholamines followed the order isoproterenol greater than epinephrine greater than norepinephrine. (c) Alprenolol, a beta-adrenergic antagonist, but not phentolamine, an alpha-antagonist, abolished the effect. (d) The maximal effects of isoproterenol and cholera toxin, an activator of adenylate cyclase, were not additive. These results suggest that under certain physiological states catecholamines may play an important role in the regulation of cholinergic receptors.

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Inhibitors of membrane depolarization regulate acetylcholine receptor synthesis by a calcium-dependent, cyclic nucleotide-independent mechanism

Cited by 28 publications

References 14 publications

Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

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

ß‐Adrenergic Receptor Activation Increases Acetylcholine Receptor Number in Cultured Skeletal Muscle Myotubes

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