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At least 235 records · Page 13Linked to original sources
PubMed1985

Interaction of the neuromuscular blocking drugs alcuronium, decamethonium, gallamine, pancuronium, ritebronium, tercuronium and d-tubocurarine with muscarinic acetylcholine receptors in the heart and ileum.

Neuromuscular blocking drugs have a high affinity for muscarinic acetylcholine receptors in the heart atria and ileal smooth muscle. In experiments on homogenates, alcuronium, gallamine, pancuronium, tercuronium and ritebronium inhibited the binding of the muscarinic antagonist (3H)quinuclidinyl benzilate (QNB) to rat heart atria with IC50 values of 0.15-0.53 mumol X 1(-1) and to ileal longitudinal muscles with IC50 values of 0.12-0.45 mumol X 1(-1). d-Tubocurarine and decamethonium inhibited (3H)QNB binding to these tissues with IC50 values of 6.2-8.5 mumol X 1(-1). For each neuromuscular blocking drug, the IC50 values were virtually identical for (3H)QNB displacement in the homogenates of the atria and of the ileal muscle. Alcuronium and gallamine differed from the other blocking agents in that they produced less steep (3H)QNB displacement curves both in the atria and the ileal muscle; Hill coefficients for the binding of alcuronium and gallamine to atrial and ileal homogenates were lower than unity. On isolated atria, gallamine, pancuronium, ritebronium and tercuronium antagonized the inhibition of tension development caused by the muscarinic agonist, methylfurmethide, with Kd values which were of the same order of magnitude as the IC50 values for the displacement of (3H)QNB binding to homogenates; the Kd of alcuronium was 12.5 times higher. d-Tubocurarine and decamethonium did not antagonize the effects of methylfurmethide at concentrations up to 100 mumol X 1(-1). On isolated ileal longitudinal muscle, gallamine and pancuronium antagonized the effects of methylfurmethide with Kd values that were 53 times and 100 times higher than their respective Kd values in the atria.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcuronium↗
PubMed1975

An analysis of the dose-response curve at voltage-clamped frog-endplates.

The agonist concentration--endplate conductance relation was examined for a number of agonists (such as carbachol, alkyl trimethylammonium salts, choline and decamethonium). The endplate current evoked varied as Imax [a/(a + K)]2, where a is the agonist concentration and Imax and K are agonist-specific parameters. This finding suggests that the endplate receptor has 2 equivalent subunits which bind agonist approximately non-cooperatively. The liganded subunits then switch to an active conformation with a probability that depends on the nature of the agonist. Both subunits must adopt the active conformation for the channel to open, but the transitions of the subunits could be either independent or concerted.

Animals↗
PubMed1976

Voltage dependence of agonist responses at voltage-clamped frog endplates.

The conductance increment produced at voltage clamped frog endplates by various agonists, applied either iontophoretically or in the bath, increases exponentially with membrane hyperpolarisation, an e-fold change being obtained with shifts of the order of 100 mV. The voltage dependency of this increase is the same for different, but low, agonist concentrations. However, conductance changes evoked by decamethonium increased less with hyperpolarisation than did conductance changes evoked by carbachol or tetramethylammonium. Hyperpolarisation slowed iontophoretic responses to carbachol or decamethonium, and enhanced and prolonged inhibition of carbachol by a brief pulse of decamethonium.

Animals↗
PubMed1989

Localization of mechanoreceptors in the protozoan, Stentor coeruleus.

Mechanoreceptor channels were localized by using the ligands, tubocurarine (TC), decamethonium (Deca), and gallamine (Gall), which have been shown to bind specifically to these channels. The binding of radioactively labeled TC (TC*) was found to be directly proportional to the cell surface area suggesting that the channels are uniformly distributed over the cell surface. Intracellular TC and Gall injections did not depress mechanical stimulus sensitivity though these drugs did depress sensitivity when applied extracellularly at the same concentrations; therefore, the ligand binding sites are on or near the external surface of the cell. Autoradiographs revealed that radioactively labeled Deca (Deca*) bound to the pigmented stripes but not to the ciliary stripes or membranellar band. Further, Stentor induced to shed their membranellar band through exposure to 8% urea were more sensitive to mechanical stimuli than were controls; therefore, the membranellar cilia do not appear to contain mechanoreceptor channels. Collectively, these data indicate that the mechanoreceptor channels are located in the somatic surface covering the pigmented stripes. The density of mechanoreceptor channels in the plasma membrane covering the somatic surface is tentatively estimated to be between 5500 and 14,500 microns-2 based on the density of TC* binding, the apparent number of TC molecules binding per mechanoreceptor channel, and data suggesting that only one fifth to one fourth of the bound TC* is bound to structures in the plasma membrane.

Animals↗
PubMed1993

Calcium influxes and calmodulin modulate the expression and physicochemical properties of acetylcholinesterase molecular forms during development in vivo.

1. Acetylcholinesterase (AcChoE; EC 3.1.1.7) exists in several molecular forms that may be anchored to cell membranes or associated with extracellular matrix. AcChoE bound to lipidic membranes is detergent extractable (DE AcChoE), whereas the enzyme associated with extracellular matrix is high salt soluble (HSS AcChoE). The latter variant is accumulated in synaptic regions by an unknown mechanism. 2. We have suggested previously that depolarization-induced Ca2+ influx is a major factor that modulates AcChoE synthesis in vivo, as well as the conversion of some DE AcChoE to HSS variant. In the present study, we have examined (i) the effects of depolarization-induced skeletal muscle inactivity and ionophore-induced Ca2+ influxes on the expression of AcChoE molecular forms and (ii) the hypothesis that Ca(2+)-dependent calmodulin may be involved in the conversion of at least some forms of DE AcChoE to HSS variant in vivo. 3. Chick embryos were treated in ovo during the early period of nerve-muscle interactions with d-tubocurarine (dTC; a competitive neuromuscular blocking agent) or with decamethonium (dMET; a depolarizing agent). Both dTC and dMET equally and significantly reduced embryonic neuromuscular activity (motility). However, dTC significantly decreased AcChoE overall activity, whereas dMET had virtually no effect on AcChoE expression, compared to controls. 4. Treatment of embryos with the Ca2+ ionophore A23187 significantly increased the total AcChoE activity as well as the DE/HSS ratio of each AcChoE molecular form. However, treatment with N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide (also termed W-7), a calmodulin antagonist, did not alter the total AcChoE activity, but significantly increased the DE/HSS ratio of AcChoE forms. 5. These results support the idea that (i) depolarization and/or Ca2+ influxes, but not muscle contraction, may regulate AcChoE expression in skeletal muscle and (ii) Ca(2+)-dependent calmodulin activation may be involved in the conversion of some DE AcChoE to their HSS variant in vivo.

Acetylcholinesterase↗
PubMed1977

Reexamination of carbodiimide as a possible affinity label for the acetylcholine receptor at the frog neuromuscular junction.

The effects of water-soluble carbodiimide were examined at the frog neuromuscular junction. Acetylcholine sensitivity was measured using a fluid electrode technique and intracellular recording of miniature end-plate potentials. The carbodiimide blocked synaptic sensitivity by a reversible, curare-like action. Irreversible blockade was also observed, probably due to covalent binding. The conditions of reaction and irreversibility suggest that several different residues may be attacked. The inability of cholinergic antagonists to protect the receptor from attack indicates that nonspecific sites, and not the acetylcholine binding site, are involved.

Acetylcholine↗
PubMed1987

Effects on transport of rapidly penetrating, competing substrates: activation and inhibition of the choline carrier in erythrocytes by imidazole.

The properties of the choline transport system are fundamentally altered in saline solution containing 5 mM imidazole buffer instead of 5 mM phosphate: (i) The system no longer exhibits accelerated exchange. (ii) Choline in the external compartment fails to increase the rate of inactivation of the carrier by N-ethylmaleimide. (iii) Depending on the relative concentrations of choline and imidazole, transport may be activated or inhibited. The maximum rates are increased more than fivefold by imidazole, but at moderate substrate concentrations activation is observed with low concentrations of imidazole and inhibition with high concentrations. (iv) The imidazole effect is asymmetric, there being a greater tendency to activate exit than entry. All this behavior is predicted by the carrier model if imidazole is a substrate of the choline carrier having a high maximum transport rate but a relatively low affinity, and if imidazole rapidly enters the cell by simple diffusion, so that it can add to carrier sites on both sides of the membrane. Addition at the cis side inhibits, and at the trans side activates. According to the carrier model, asymmetry is a necessary consequence of the potassium ion gradient in red cells, potassium ion being another substrate of the choline system.

Biological Transport↗
PubMed1982

The effect of cholinergic antagonists on a central response to nicotine.

Mecamylamine and hexamethonium antagonize the prostration response of rats to centrally-administered nicotine; decamethonium and d-tubocurarine are less effective. physostigmine does not elicit the response. Nicotine's central cholinergic effect thus may contribute to but does not fully account for its action.

Animals↗
PubMed1976

Junctional and extrajunctional acetylcholine receptors in normal and denervated frog muscle fibres. Noise analysis experiments with different agonists.

Ionic channel properties of acetylcholine receptors located in, in the vicinity of, or far away from a frog neuromuscular junction were investigated by noise analysis of drug induced current fluctuations. For drugs applied to the junction, in certain cases two Lorentzian curves were necessary to describe the data. It is postulated that the reason for this observation is that a contribution from perijunctional receptors was being observed. The conductance of a single channel in the junction was independent of the nature of the agonist and had an average value of 17.9 pS (temperature range 8-25 degrees C, solution buffered with Tris). After denervation for 21 days the conductance gamma was 7.5 pS at extrajunctional locations. In the close neighbourhood of the junction (peri-junctional receptors) values were found between 4 and 19 pS. The mean value of the open channel life-time tau in the endplate exposed to acetylcholine was 2.4 ms at 8-11 degrees C. This value was 0.90 ms with carbachol, 0.50 ms with succinylcholine, 0.28 ms with decamethonium and 0.45 ms with nicotine. The receptors outside the endplate exhibited tau-values which at a given temperature were 2-3 times larger than those at the endplate. Raising the temperature to 23 degrees C reduced all tau-values by factors of 2-3. It is concluded that at least two types of ACh-receptors with different properties exist in the muscle membrane, possibly produced by ACh-receptive units in different states of aggregation.

Acetylcholine↗