[L-glutamate--a candidate for the role of membrane-potential nerve control factor in mammalian muscle fibers].

L-glutamate released from the motor nerve terminal seems to be involved in the maintenance of resting potential (RP) in skeletal muscles via the N-methyl-D-aspartate (NMDA)-activated influx of Ca2+ to the cytoplasm with subsequent activation of NO-synthase and production of the NO which could act as a messenger providing the control of the membrane ion-transporting proteins.

[Is transferrin a neurotrophic factor controlling myosin composition of the skeletal muscle?].

After transferrin injection to the slow m. soleus of guinea pig no immunohistochemical changes in myosin composition with monoclonal antibodies (AB) against fast myosin heavy chain (HCf) have been found. All muscles fibers in intact and experimental animals were identified as slow ones (type I of muscle fibers).

[Neurotrophic control of myosin synthesis in guinea pig slow muscle].

After experimental cease of neurotrophic control of skeletal muscle by denervation no changes in myosin ATP-ase histochemistry and immunohistochemical profile in slow (m. soleus) muscle of guinea pig were found. All muscle fibers in intact muscle fibers).

[Neurotrophic control of the ionic regulation mechanisms for intracellular water content in muscle fibers of mammals].

The volume change of the muscle fibres in the hypertonic medium begins with cell shrinkage. Later the cell volume increases up to the normal level because of the furosemide-sensitive CL(-)-influx activation. The property of the Cl(-)-influx to be activated in the hypertonic medium is abolished after denervation.

[Effects of hyperosmolarity and furosemide on resting membrane potentials and skeletal muscle fiber volume in rats].

The changes of the muscle fibres volume and resting membrane potential (RMP) were studied following treatment with hypertonic medium and furosemide. The volume changes in hypertonic medium began with cell shrinkage and later have been followed by the volume increase up to normal level during 30-40 minutes. At the same time the medium hypertonicity caused muscle fibres depolarisation.

[Effects of death of a single neuron on the functional organization of the neuronal ensemble in the leech].

The reaction of leech nervous system after elimination of individual mechanosensory neuron by intracellular Pronase injection were studied. In the motor neurons connected with killed cells at 14-90th days after the operation there were the changes of the resting membrane potential and amplitude of postsynaptic potentials developed by the stimulation of mechanosensory neuron. It is suggested that the leech nervous system serves as the dynamic formation depending on changes of neuronal ensemble structure.

[The electrical and contractile activity of denervated smooth muscle].

The effect of norepinephrine, histamine, serotonin and potassium chloride on electrogenesis and contraction was studied on innervated and denervated smooth muscles of cat's nictitating membrane. Denervated smooth muscles generate slow depolarizing potentials with the APs corresponding to tonic and phasic contractions, resp. Tonic contractions occur with no considerable change fo the MP in innervated muscles, phasic contractions being absent.

[Simulation of the neurotrophic control of the resting membrane potential in rat skeletal muscle by using electrical stimulation and an exogenous cholinomimetic].

Decrease of the resting MP caused by denervation of the rat diaphragm muscle, was studied in vitro. Addition of carbamylcholine as well as electrical stimulation hyperpolarized the muscle membrane, the effect of the former being not prevented by d-tubocurarine. The hyperpolarizing effects of carbamylcholine and electrical stimulation used simultaneously were not added up.

[Role of opioid peptides in the neurotrophic control of the acetylcholine-sensitive membrane of rat skeletal muscle fibers].

The influence of opiate peptides on the development of hypersensitivity to acetylcholine has been revealed in muscle fibers membrane after denervation of rat diaphragm muscle. The addition of 1 X 10(-8) M beta-endorphin or dalargin to the culture medium prevented the appearance of extra-junctional acetylcholine sensitivity. The peptide containing only three amino acids and identical to the initial dalargin region did not possess the same effect.

[Effect of acetylcholine and carbamylcholine on the resting membrane potential of denervated muscle in the rat].

The decrease of resting MP after denervation in diaphragm muscle of the rat was studied in vitro. Transitory activation of Na+,K+-pump by carbamylcholine, acetylcholine or adrenaline hyperpolarized the muscle fiber membrane but did not compensate the postdenervation fall of the MP. Similarly, the permanent presence of carbamylcholine at culturing media did not prevent the development of changes in the MP after denervation.

[Neurotrophic control of transmembrane chlorine transport in the muscle fibers of mammals].

The resting membrane potential of innervated and denervated rat diaphragm muscle fibres was studied at different concentrations of Cl-, K+ and Na+ in the external solution and following the furosemide treatment. The Cl- equilibrium potential (ECl) and resting potential are equal in innervated fibres while denervation shifts the ECl value in the positive direction when compared with the resting potential value. The postdenervation depolarization is delayed in furosemide-treated muscles.

[Effect of beta-endorphin on the development of denervation changes in the membrane of the muscle fiber in the rat].

A decrease in the resting membrane potential, an increase in the input resistance, appearance of the anode breakdown and tetrodotoxin-resistant action potentials and extrajunctional acetylcholine sensitivity following denervation were revealed in surviving rat diaphragm muscle fibres. Addition of beta-endorphin (1.10(-8) M) to the culture medium prevented on increase in the input resistance and reduced a degree of the extrajunctional acetylcholine sensitivity, but did not inhibit the appearance of the anode breakdown and tetrodotoxin-resistant action potentials.

[Importance of calcium ions and impulse activity for neurotrophic control of the membrane potential of muscle fibers in the rat].

The blockade of the Ca++ influx increased the postdenervation depolarization of the membrane potential in rat diaphragm muscle fibres, while elevation of the intracellular Ca++ content by caffeine hyperpolarized the muscle membrane. Direct electrical stimulation of muscle or application of carbamylcholine reduced the degree of postdenervation membrane depolarization. Verapamil and d-tubocurarine abolished the hyperpolarizing effect of the electrical stimulation.

[Effect of disruption of chloride conductance on the development of denervation changes in muscle fiber membranes of the rat].

A decrease in resting MP, increase in the input resistance, appearance of anode breakdown APs, and extrajunctional acetylcholine sensitivity following denervation were revealed in the rat diaphragm muscle fibres. Addition of 1 X 10(-4) M furosemide to the culture medium reduced the degree of post-denervation muscle membrane depolarization and of extrajunctional acetylcholine sensitivity, but did not prevent the changes in passive electrical properties and in firing level of the muscle fibre membrane. Chloride ions could serve as intracellular messengers responsible for the neurotrophic control of muscle membrane resting potential and membrane sensitivity to acetylcholine.

[Role of calcium ions and cyclic nucleotides in neurotrophic control of the membrane properties of muscle fibers in the frog].

Subcutaneous injections of caffeine, calcium ionophore X537A or cAMP did not affect the changes of input resistance (R0) and time constant (T) of membrane caused by denervation of the frog m. sartorius but prevented the MP decrease and ACh sensitivity spread. Injections of cGMP did not affect the denervation changes of R0 and MP but increased the ACh sensitivity.

[Effect of hydrocortisone on neuromuscular transmission in the frog skeletal muscles].

Hydrocortisone (1.10(-7)-1.10(-5) M/l) in vitro experiments on frog's muscle in conditions of preliminary curarization increases dose-dependently the quantum content of e.

[Does non-quantum secretion of acetylcholine from motor neuron endings participate in the neurotrophic control of the membrane potential of muscle fibers in the rat?].

The resting membrane potential of synaptic zone of muscle fibres within 2-3 mm (near) and 9-11 mm (far) of the nerve section of the rat diaphragm muscle was measured after 3 hours or on the 5th day after the motor nerve section. The membrane potential of "near" fibres was lower than that of "far" fibres. The presence of carbamylcholine or cGMP in the culture medium maintained the membrane potential of "near" fibres close to that of "far" fibres.

[Effect of blockade of axonal transport on endplate currents of muscle fibers in the frog].

The evoked and spontaneous end-plate currents (EPC) were measured in normal voltage-clamped frog sartorius muscle fibres and after colchicine blockade of axoplasmic transport in the corresponding nerve. Colchicine application decreased the growth rate and increased the decay time constant of EPC without changes in the average amplitude of EPC and miniature EPC, quantum content of EPC and frequency of miniature EPC. The increase in EPC time constant was combined with an increase in the sensitivity of the time constant to holding potential, but there were no changes in the amplitude of EPC as a function of holding potential in the reversal potential of EPC.

[Effect of hydrocortisone on the membrane properties of innervated and denervated muscle fibers in frogs].

Two injections of 10, 100 or 1000 micrograms of hydrocortisone into the lymphatic sack with one-week interval or daily injections of 100 micrograms of the hormone did not hinder a decrease in the membrane resting potential, an increase of the input resistance and time constant of the membrane as well as appearance of nonsynaptic sensitivity to acetylcholine in muscle fibers developing by the 13-15th day after denervation of the muscle. In latter two cases, however, no increase of the input resistance and time constant of the membrane occurs. Administration of the same doses of drug to intact frogs led to a decrease of the membrane resting potential, increase of the time constant and input resistance of the membrane whereas daily injections reduced the sensitivity of muscle fibers to acetylcholine.

[Effect of motor function disorder on the properties of the muscle fiber membrane].

Experiments on frogs with the use of the microelectrode techniques were made to study the effect of tenotomy and immobilization of a limb with a metal cast in the extension position on the properties of the membrane of muscle fibers. Two weeks after tenotomy there were no changes in the magnitude of the membrane rest potential, input resistance and time constant of the membrane of muscle fibers or in the pattern of its sensitivity to acetylcholine. Two and three weeks after the limb immobilization no changes in the membrane rest potential and passive electrical properties of the muscle membrane were recorded either.

[Non-quantum secretion of acetylcholine in a nerve-muscle preparation of the diaphragm in dystrophic mice of line 129/Rej].

Experiments were carried out on phenotypically normal and sick homozygotic 129/Rej mice suffering from congenital dystrophy. The membrane rest potential (MRP) for muscle fibers of sick homozygotic animal diaphragm appeared lower than that of phenotypically normal species, attesting to the denervation-like pattern of muscle pathology. After muscle treatment with armine, and irreversible acetylcholinesterase inhibitor, d-tubocurarine chloride hyperpolarized the postsynaptic membrane without affecting the MRP of the extrasynaptic zone of muscle fibers.

[Neurotrophic control of the mechanism of action potential generation in frog muscle fibers].

Muscle denervation or blockade of axoplasmic transport with colchicine exert no effect on the AP rate of rise, or phase of repolarization, amplitude of overshoot, critical revel of depolarization, or their sensitivity to tetrodotoxin in frog skeletal muscle fibers. But under these conditions the difference in the rate of AP rise in sensitive and insensitive to acetylcholine zones of muscle's membrane disappears, APa become resistant against ouabain, and 36% of examined fibers display rhythmic spike activity after a single depolarizing stimulum. Adrenaline increases and high Ca2+ concentration or disruption of muscle fiber's sarcoplasmic tubules in opposite side decrease the number of fibers with the rhythmic spike activity.

[Effect of postsynaptic blockade of neuromuscular transmission on membrane properties of phasic muscle fibers in the frog].

Electric properties and acetylcholine sensitivity in frog sartorius muscle fibres were investigated after denervation and after prolonged paralysis with d-tubocurarine and alpha-bungarotoxin. No changes similar to those that appeared after nerve section developed in the muscle fibres after d-tubocurarine or alpha-bungarotoxin treatment. It is suggested that neurotrophic control of muscle fibres in frog is supported by materials transported to the muscle by axoplasmic flow rather than by the junctional acetylcholine or nerve impulsation.

[Role of the sympathetic nervous system in neurotrophic control of the muscle fiber membrane in frogs].

Surgical desympathization of skeletal muscle fibre does not change the resting membrane potential or input resistance of muscle fibre membrane, but induces extrajunctional sensitivity to acetylcholine though lesser by half than that after anatomical muscle denervation. Raucedil injection and nerve stump transplantation on the muscle do not cause any changes in muscle membrane. The data obtained suggest the sympathetic nervous system participation in neurotropic control of muscle membrane sensitivity to acetylcholine.