Axotomy-induced loss of m2 muscarinic receptor mRNA in the rat facial motor nucleus precedes a decrease in concentration of muscarinic receptors

1996 ◽  
Vol 28 (11) ◽  
pp. 771-778 ◽  
Author(s):  
Donald B. Hoover ◽  
Ronald H. Baisden ◽  
James V. Lewis
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Motor Nucleus ◽  
Receptor Mrna ◽  
Facial Motor Nucleus ◽  
M2 Muscarinic Receptor

Neuromuscular Relaxants as Antagonists for M2and M3Muscarinic Receptors 

1998 ◽  
Vol 88 (3) ◽  
pp. 744-750 ◽  
Author(s):  
Vivian Y. Hou ◽  
Carol A. Hirshman ◽  
Charles W. Emala
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Radioligand Binding ◽  
Chinese Hamster ◽  
Neuromuscular Relaxants ◽  
Ovary Cell ◽  
Relative Order ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
M3 Muscarinic Receptor

Background Neuromuscular relaxants such as pancuronium bind to M2 and M3 muscarinic receptors as antagonists. Blockade of muscarinic receptors in atria of the M2 subtype mediates tachycardia. In the lung, blockade of M2 receptors on parasympathetic nerves potentiates vagally induced bronchospasm, whereas blockade of M3 receptors on bronchial smooth muscle inhibits bronchospasm. The current study was designed to quantify the affinity of a series of neuromuscular relaxants for the M2 and M3 muscarinic receptors, which were individually stably transfected in Chinese hamster ovary cell lines. Methods Competitive radioligand binding assays determined the relative binding affinities of the neuromuscular relaxants pancuronium, succinylcholine, mivacurium, doxacurium, atracurium, rocuronium, gallamine, and pipecuronium for the muscarinic receptor in the presence of a muscarinic receptor antagonist (3H-QNB) in membranes prepared from cells individually expressing either the M2 or M3 muscarinic receptor. Results All muscle relaxants evaluated displaced 3H-QNB from muscarinic receptors. The relative order of potency for the M2 muscarinic receptor (highest to lowest) was pancuronium, gallamine, rocuronium, atracurium, pipecuronium, doxacurium, mivacurium, and succinylcholine. The relative order of potency for the M3 muscarinic receptor (highest to lowest) was pancuronium, atracurium, pipecuronium, rocuronium, mivacurium, gallamine, succinylcholine, and doxacurium. Conclusions All neuromuscular relaxants studied had affinities for the M2 and M3 muscarinic receptor, but only pancuronium and gallamine had affinities within the range of concentrations achieved with clinical use. The high affinities of gallamine and pancuronium for the M2 muscarinic receptor are consistent with a mechanism of M2 receptor blockade in relaxant-induced tachycardia.

Ozone-induced airway hyperresponsiveness and loss of neuronal M2 muscarinic receptor function

1994 ◽  
Vol 76 (3) ◽  
pp. 1088-1097 ◽  
Author(s):  
A. H. Schultheis ◽  
D. J. Bassett ◽  
A. D. Fryer
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Ozone Exposure ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
Release Of Acetylcholine ◽  
M2 Muscarinic Receptors

The effect of acute ozone exposure on the function of efferent parasympathetic nerves, M3 muscarinic receptors on airway smooth muscle, and inhibitory M2 muscarinic receptors on the parasympathetic nerves was studied. Immediately after exposure to 2.0 ppm ozone for 4 h, guinea pigs became hyperresponsive to electrical stimulation of the vagus nerves. The normal airway response to intravenous cholinergic agonists at this time demonstrates normal M3 receptor function. M2 muscarinic receptors on the nerves, which normally inhibit release of acetylcholine, were dysfunctional after ozone exposure, as demonstrated by the failure of the muscarinic agonist pilocarpine to inhibit, and the failure of the M2 antagonist gallamine to potentiate, vagally mediated bronchoconstriction. Thus, loss of inhibitory M2 muscarinic receptor function after ozone exposure potentiates release of acetylcholine from the vagus nerves, increasing vagally mediated bronchoconstriction. By 14 days, postozone responses to vagal nerve stimulation were not different from those of air-exposed animals and the function of the neuronal M2 muscarinic receptor was normal, confirming that ozone-induced hyperresponsiveness is reversible.

Decrease in β1-adrenergic and M2-muscarinic receptor mRNA levels and unchanged accumulation of mRNAs coding for Gαi‒2 and Gαs proteins in rat cardiac hypertrophy

1995 ◽  
Vol 27 (10) ◽  
pp. 2287-2294 ◽  
Author(s):  
Adrian Mondry ◽  
Francine Bourgeous ◽  
François Carré ◽  
Bernard Swynghedauw ◽  
Jean-Marie Moalic
Keyword(s):  
Cardiac Hypertrophy ◽  
Muscarinic Receptor ◽  
Mrna Levels ◽  
Receptor Mrna ◽  
M2 Muscarinic Receptor

scholarly journals Immunocytochemical localization of M2 muscarinic receptors in rat ventricles with anti-peptide antibodies.

1994 ◽  
Vol 42 (3) ◽  
pp. 337-343 ◽  
Author(s):  
M Fu ◽  
W Schulze ◽  
W P Wolf ◽  
A Hjalmarson ◽  
J Hoebeke
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Receptor Protein ◽  
Extracellular Loop ◽  
Electron Microscopic ◽  
Major Band ◽  
Rat Cardiomyocytes ◽  
M2 Muscarinic Receptor ◽  
T Tubules ◽  
M2 Muscarinic Receptors

We produced antibodies against a synthetic peptide corresponding to amino acids 168-192 of the second extracellular loop of the M2 human muscarinic receptor in rabbits. In immunoblot, affinity-purified antibodies specifically recognized a major band of rat ventricular muscarinic receptor protein with a molecular weight of about 80 KD. This recognition could be blocked by pre-incubation with peptide. Moreover, with both light (LM) and electron microscopic (EM) immunocytochemistry techniques, muscarinic receptors were detected on sarcolemma and T-tubules of rat cardiomyocytes. In addition, immunoreactions were localized in membranes of capillaries. Likewise, these reactivities were abolished by pre-incubation with peptide. These results suggest that the antibodies against the second extracellular loop of human M2 muscarinic receptor could specifically recognize rat ventricular muscarinic receptor protein and could be a powerful tool to study the fate of this receptor under different pathological or physiological conditions.

Ozone-induced loss of neuronal M2 muscarinic receptor function is prevented by cyclophosphamide

1994 ◽  
Vol 77 (3) ◽  
pp. 1492-1499 ◽  
Author(s):  
L. M. Gambone ◽  
C. L. Elbon ◽  
A. D. Fryer
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Ozone Exposure ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
M2 Muscarinic Receptor ◽  
M2 Muscarinic Receptors

We tested the hypothesis that inflammatory cells mediate the loss of neuronal M2 muscarinic receptors in the lung after ozone exposure. Pathogen-free guinea pigs treated with cyclophosphamide (30 mg.kg-1.day-1 i.p. for 7 days) before exposure to ozone were compared with untreated ozone-exposed animals. This dose of cyclophosphamide significantly reduced leukocytes in peripheral blood and bronchoalveolar lavage fluid. Twenty-four hours after ozone, muscarinic receptor function was tested in anesthetized animals. In air-exposed guinea pigs, vagally induced bronchoconstriction was attenuated by the muscarinic agonist pilocarpine (0.1–100 micrograms/kg i.v.) and potentiated by the selective M2 antagonist gallamine (0.1–10 mg/kg i.v.), indicating that the neuronal M2 muscarinic receptors were functioning. These responses were significantly reduced after ozone, indicating loss of neuronal M2 muscarinic receptor function. However, in those animals treated with cyclophosphamide, M2 muscarinic receptor function was not altered by ozone. These data suggest that ozone-induced loss of neuronal muscarinic receptor function is mediated via inflammatory cells and that the link between ozone-induced hyperresponsiveness and inflammation may be the neuronal M2 muscarinic receptor.

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