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At least 37 records · Page 2Linked to original sources
PubMed1975

Correlation between drug induced changes of acetylcholine release and acetylcholine fractions in rat brain.

After administration of eserine, a new acetylcholine (ACh) subfraction called f+ is formed in rat brain tissue. References and methods are given for the calculation of this subfraction, which can be isolated and determined only together with the so-called "free" ACh fraction. Alterations of the f+-ACh subfraction caused by barbital, urethane, pentetrazol, arecoline and scopolamine in telencephalon, cortex and striatum of rat brain are connected with changes of ACh concentrations determined in comparable releasing tests.

Acetylcholine↗
PubMed1992

Crosslinking of proteins in acetylcholine receptor-rich membranes from Torpedo californica: relation of 43-kD protein and Torpedo dystrophin to acetylcholine receptor.

We examined the spatial relation of 43-kD protein and Torpedo dystrophin, which are cytoplasmic peripheral membrane proteins in the nicotinic acetylcholine receptor (AChR)-rich membranes, to AChR. We used three kinds of the heterobifunctional crosslinking reagents to crosslink proteins in the AChR-rich membranes. Products crosslinked by SMPB (14.5 A span) including 43-kD protein and Torpedo dystrophin appeared at the tops of the stacking gels at the concentrations of 8.89 x 10(-5)M to 8.89 x 10(-3)M SMPB. High molecular weight materials (crosslinked products) increased with increasing concentrations of the crosslinker. On the other hand, band intensity of alpha, beta, and delta subunits of AChR remained unchanged up to a concentration of 2.67 x 10(-3)M SMPB, while the band of gamma subunit diminished at the same concentrations as did that of the 43-kD protein. Torpedo dystrophin was also crosslinked at the same concentrations as were effective for the 43-kD protein and gamma subunit. On the basis of these results, we conclude that the 43-kD protein is intimately associated with the gamma subunit of AChR and Torpedo dystrophin.

Animals↗
PubMed1977

Pancreatic acinar cells: localization of acetylcholine receptors and the importance of chloride and calcium for acetylcholine-evoked depolarization.

1. Intracellular micro-electrode recordings of acinar cell membrane potential and resistance were made from the mouse pancreas superfused in vitro. The acinar cells under investigation were stimulated by micro-iontophoretic ACh application from an extracellular AChCl-filled micro-electrode.2. Passing short-lasting ejecting current pulses through the AChCl-electrode caused acinar cell depolarization when the electrode was in an extracellular position not far (< 50 mum) from an acinus impaled by a KCl micro-electrode. After insertion of the AChCl electrode into a neighbouring acinar cell, electrically coupled to the acinar cell already impaled by the KCl-electrode, ejecting ACh current pulses only affected the membrane potential in a direct electrical manner whereas there was no sign of an effect of ACh on the membrane potential.3. Replacing extracellular chloride by sulphate caused a marked increase in the amplitude of the ACh-evoked depolarization. If the membrane potential was recorded with a KCl electrode ACh continued to evoke very large depolarizations even after more than 1 hr exposure to Cl-free solution. If the membrane potential was recorded with a K-citrate electrode the effect of Cl-removal was only transient. Removal of Na(+) during exposure to Cl-free solution reduced the amplitude of the ACh-evoked depolarization somewhat. Readmission of Cl after more than 1 hr of Cl deprivation caused an immediate reversal of the ACh effect into a hyperpolarization.4. Removal of extracellular Ca(2+) caused a marked reduction in the amplitude of small depolarizations evoked by just suprathreshold doses of ACh, whereas there was very little effect on larger depolarizations evoked by maximal or supramaximal ACh ejections. The effect of Ca removal was fully reversible. Addition of Mn after Ca-deprivation was as efficient as Ca in restoring normal electrophysiological responses to small doses of ACh.5. The acinar cell membrane seems only to be responsive to ACh added to the extracellular side and ACh probably causes an increase in membrane Cl permeability in addition to the previously described effects on Na and K permeability. Ca may be important in determining ACh receptor sensitivity.

Acetylcholine↗
PubMed1977

Modulation of acetylcholine receptor by antibody against the receptor.

Antibody against acetylcholine receptor induces an increase in the rate of degradation of acetylcholine receptors on a mouse cell line (BC(3)H-1) and cultured rat skeletal muscle. The increased rate of degradation results in a lowered density of acetylcholine receptors on muscle membrane and a lowered sensitivity to iontophoretically applied acetylcholine. The modulation of acetylcholine receptor is energy, temperature, and time dependent and may be related to antigenic modulation found in other systems. Acetylcholine noise analysis demonstrates that antibody against acetylcholine receptor reduces the channel mean conductance and mean open time slightly. It is concluded that antibody binds to the acetylcholine receptor, impairs its function, and induces receptor degradation. This results in a lowered density of acetylcholine receptor and a lowered sensitivity to acetylcholine. Patients with myasthenia gravis have antibodies to their acetylcholine receptor in their serum. Antigenic modulation of receptor in the muscle of patients with myasthenia gravis could contribute to the observed decrease in amplitudes of miniature endplate potentials and in muscle acetylcholine sensitivity, and the symptoms of muscular weakness.

Acetylcholine↗
PubMed1975

Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips.

1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibitor. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g times min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55 per cent, respectively. 3. Oxotremorine (10-5 and 10-4M) significantly inhibited the resting release of acetylcholine by 25 and 33 per cent, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3 times 10-7 M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetycholine concentration. In in vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of exotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.

Acetylcholine↗
PubMedDate not supplied

Further evidence that extrinsic acetylcholine acts preferentially on extrajunctional receptors in the chick biventer cervicis muscle.

The specificity of action of extrinsic acetylcholine on extrajunctional and junctional receptors in the chick biventer cervicis muscle was studied by determining its ability to protect the responses evoked by acetylcholine and by tetanic nerve stimulation from the blockade by alpha-bungarotoxin, an irreversible binding agent of acetylcholine receptors. At concentrations of 50-100 mug/ml, acetylcholine caused a desensitization to extrinsic acetylcholine but not to nerve stimulation and protected only the contractile response to extrinsic acetylcholine from the toxin blockade whereas neither the response to tetanic nerve stimulation nor the endplate potentials were protected. For the protection of the latter, higher concentrations of acetylcholine were needed. In the presence of physostigmine, a concentration of acetylcholine as low as 10 mug/ml protected the endplate potentials from the toxin blockade. By contrast, d-tubocurarine protected the tetanic contraction and the endplate potentials induced by nerve stimulation at a concentration which produced the same protection of acetylcholine-induced contraction as that produced by 50-100 mug/ml acetylcholine. These results indicate that in contrast to d-tubocurarine, extrinsic acetylcholine at low concentrations acts preferentially on the extrajunctional receptors in the absence of an anticholinesterase.

Acetylcholine↗
PubMed1991

Differences in the K(+)-channels opened by cromakalim, acetylcholine and substance P in rat aorta and porcine coronary artery.

1. The effects of acetylcholine and substance P on the efflux of 86Rb+ and 42K+ from rat aorta and pig coronary artery, respectively, were compared with those of the K+ channel opening agent, cromakalim. 2. In rat aorta preloaded with 86Rb+ and/or 42K+, acetylcholine produced transient, concentration-dependent increases in the efflux rate coefficients of these tracers (maximum approximately 35%). These effects were abolished by endothelial cell removal. 3. Donor/acceptor experiments with rat aorta suggested that at least some of the efflux of 86Rb+ seen in the presence of acetylcholine was not derived from the endothelium, but came from the smooth muscle itself. 4. Acetylcholine (10 microM)-induced 86Rb+ efflux was reduced by tetraethylammonium (TEA, 10 mM) to 33% and ouabain (300 microM) to 54% of control. Preincubation with Ba2+ (100 microM) did not significantly inhibit acetylcholine-induced efflux. 5. Acetylcholine-induced 42K+/86Rb+ efflux was unaffected by preincubation with glibenclamide (10 microM). In contrast, the 42K+/86Rb+ efflux induced by cromakalim was inhibited by glibenclamide (50 nM) by 50%. 6. Acetylcholine (0.3-10 microM)-induced inhibition of phenylephrine (1 microM)-induced tone was abolished by endothelial cell removal but unaffected by glibenclamide. Cromakalim-induced relaxations were endothelium-independent and were inhibited by glibenclamide in a concentration-dependent manner. 7. LG-monomethyl L-arginine (L-NMMA, 250 microM) produced a significant (37 +/- 14%) inhibition of acetylcholine-induced 86Rb+ efflux whereas DG-monomethyl L-arginine was without effect. In the tissue bath L-NMMA inhibited relaxations produced by acetylcholine (0.3-10 microM), but was without effect on responses to cromakalim. 8. In the pig coronary artery, substance P induced an endothelium-dependent efflux of 86Rb+ and 42K+, which was unaffected by preincubation with glibenclamide (10 microM) or L-NMMA (250 microM). 9. The present study shows that acetylcholine and substance P each open K(+)-channels in arterial smooth muscle. However, the insensitivity of the stimulated 86Rb/42K+ efflux to inhibition by glibenclamide suggests that the K(+)-channel opened by these agents is different from the K(+)-channel opened by cromakalim. In addition, the inability of L-NMMA to inhibit fully the acetylcholine- and substance P-stimulated 86Rb+ efflux suggests that in rat aorta and pig coronary artery the endothelium-derived hyperpolarizing factor(s) (EDHF) is different from endothelium-derived relaxing factor (EDRF).

Acetylcholine↗
PubMed1978

[Pharmacological studies on supersensitization (IV). Site and mode of action of cocaine to potentiate acetylcholine in isolated tracheal preparation of rat (author's transl)].

Effects of cocaine on acetylcholine-induced contracture of isolated rat tracheal preparation were determined. The sensitivity of the preparation to acetylcholine but not methacholine and carbachol was increased by cocaine. The maximum responses induced by choline esters were not augmented by cocaine. The potentiation of acetylcholine was remarkable in calcium-deficient medium and cocaine augmented acetylcholine-contracture of the preparation suspended in calcium-free Tyrode solution. Calcium-contracture of the preparation susspended in isotonic 60 mM- or 100 mM-K+ Locke-Ringer solution was not augmented by cocaine. Extrapolating the time course of decrease in acetylcholine-contracture in calcium-free Tyrode solution, rates of calcium movement from and into calcium-stores were determined and it was found that cocaine did not change the calcium-content and rate of calcium-efflux but the rate of calcium-uptake was apparently increased with cocaine. The contribution of anticholinesterase activity of cocaine to potentiation of acetylcholine appeared negligible and the affinity of acetylcholine-receptor to acetylcholine and atropine was not changed with cocaine. Thus, cocaine increases acetylcholine-induced calcium-release and potentiates acetylcholine-contracture of isolated rat tracheal preparation.

Acetylcholine↗