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F Vyskocil

Publications and source records attributed to F Vyskocil.

157 records · Page 9Linked to original sources
PubMed1970

Dependence of acetylcholine desensitization on the membrane potential of frog muscle fibre and on the ionic changes in the medium.

1. The rate of desensitization of the post-synaptic membrane to prolonged action of acetylcholine was investigated during (a) potassium depolarization of the frog muscle fibre, (b) artificial changes of the membrane potential and (c) in the presence of some multivalent cations and of caffeine.2. Depolarization of the muscle fibre by 15 mM-K(+) led to a slowing down in the development of desensitization by 80%. This effect on desensitization produced by membrane potential changes could account for the previously described effect of increased K(+) concentration.3. Electrotonically produced depolarization of the muscle fibre membrane resulted in a decrease, hyperpolarization in an increase of the rate of desensitization.4. Several multivalent cations can be, according to their ability to increase rate of desensitization, arranged in the following series: [Formula: see text]5. Caffeine in a concentration of 1.5 mM does not affect the rate of desensitization.6. A hypothesis is presented suggesting that desensitization is not only restricted to the receptor level but that it also occurs, at least partly, at the terminal stages of the activation system.

Acetylcholine↗
PubMed1968

The effect of atropine on the frog sartorius neuromuscular junction.

1. The effect of atropine sulphate and of (+)-tubocurarine chloride (TC) on the amplitude and time course of end-plate potentials (e.p.p.s) and miniature end-plate potentials (m.e.p.p.s) was studied in the sartorius muscle of the frog.2. Atropine sulphate reduces the amplitude of intracellularly recorded e.p.p.s and m.e.p.p.s, in concentrations 100 times higher than TC (6 x 10(-5)M for 50% reduction of amplitude compared with 6 x 10(-7)M for TC).3. Atropine sulphate causes a marked shortening of both e.p.p.s and m.e.p.p.s: when the amplitude of e.p.p.s or m.e.p.p.s is reduced by 50%, their rise-time and half-decay time are both shortened by 40%. The corresponding shortening produced by TC is 15%.4. E.p.p.s prolonged by prostigmine 10(-6) g/ml. undergo a larger shortening (30%) in TC, while atropine-induced shortening related to the corresponding drop of amplitude is the same whether prostigmine is used or not.5. On repeated applications after recovery of amplitude and time course, TC loses its shortening effect on e.p.p.s while the atropine shortening effect remains unchanged.6. Atropine sulphate shortens the rise-time but not the falling phase of brief depolarizations produced by electrophoretic applications of acetylcholine (ACh) to the muscle fibre surface in the end-plate region. It also reduces their amplitude, in the same way that it reduces the amplitude of e.p.p.s.7. Atropine sulphate in concentrations which markedly reduce the amplitude and time course of e.p.p.s has no effect on their quantum content.8. Atropine sulphate at a concentration of 10(-4)M does not change the amplitude and time course of an electrotonic potential produced by a rectangular current pulse passed through the end-plate region of a muscle fibre.9. It is suggested that either enhanced removal of ACh or a spatial gradient of effectiveness of the blocking drugs, or both these mechanisms, participate in shortening the e.p.p. by atropine sulphate and TC.

Acetylcholine↗
PubMed1967

The action of tubocurarine and atropine on the normal and denervated rat diaphragm.

1. The potency with which tubocurarine chloride (TC) and atropine sulphate (AS) influence the amplitude of the end-plate potentials was measured in the rat diaphragm. This effect was compared with the action of these drugs on brief depolarizations evoked by iontophoretic application of ACh to end-plate-free spots of the chronically denervated fibre.2. TC and AS act similarly on e.p.p.s, but the concentrations necessary to cause the same effect are 2000-times higher for AS.3. The dose-response curves for both inhibitors are unchanged by prostigmine.4. Ten to twenty-five days after denervation the ACh-potentials of the sensitized end-plate-free parts of the membrane are less responsive to curare than the normal e.p.p.s are. AS is as effective in blocking ACh potentials of denervated muscles as it is in blocking normal e.p.p.s. The curare/atropine coefficient (dose ratio for equal effect) is 0.0005 for e.p.p.s and 0.003 for ACh potentials of the denervated membrane.5. Both blocking drugs reduce the amplitude of ACh-potentials evoked in the end-plate region of normally innervated rat diaphragm fibres as effectively as they reduce the amplitude of e.p.p.s.6. Neither TC nor AS have a presynaptic action in concentrations markedly reducing the e.p.p. amplitude.

Acetylcholine↗
PubMedDate not supplied

Modulation by nitric oxide (NO) of the intensity of non-quantum mediator secretion in neuromuscular junctions in rats.

Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside SNP) and S-nitroso-N-acetylpenicillamine (SNAP). as well as L-arginine. a substrate for NO synthesis. decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptors on the postsynaptic membrane by d-tubocurarine in conditions of irreversible inhibition of acetylcholinesterase with armine. Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. All these points provide evidence that NO can function as a modulator of non-quantum mediator release in the neuromuscular junctions of warm-blooded animals.

Acetylcholine↗