[L-glutamate--a candidate for the role of membrane-potential nerve control factor in mammalian muscle fibers]. / L-glutamat--pretendent na rol' faktora nervnogo kontrolia membrannogo potentsiala v myshechnykh voloknakh mlekopitaiushchikh.

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?]. / Iavliaetsia li transferin neirotroficheskim faktorom, kontroliruiushchim sostav miozinov skeletnoi myshtsy?

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). After colchicine treatment of nerve trunk innervating slow muscle, some muscle fibers reacting with monoclonal AB against myosin HCf have been found. However, after colchicine treatment of nerve trunk and transferrin injection also some muscle fibers in slow muscle reacting with monoclonal AB against myosin HCf have been found. In appears that transferrin probably can not be the factor of neurotrophic control for myosin composition in skeletal muscle.

[Neurotrophic control of myosin synthesis in guinea pig slow muscle]. / Neirotroficheskii kontrol' sinteza miozinov medlennoi myshtsy morskoi svinki.

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). However after colchicine blockade of axoplasmic transport in this slow muscle some muscle fibers reacting with monoclonal antibodies against fast myosin heavy chain were found. At the same time no changes in histochemical ATP-ase profile were observed. Validity of myosin ATP-ase histochemistry for muscle fibers typing as well as possible influence of nerve activity and neurotrophic control itself were discussed.

[Neurotrophic control of the ionic regulation mechanisms for intracellular water content in muscle fibers of mammals]. / Neirotroficheskii kontrol' ionnykh mekhanizmov reguliatsii vnutrikletochnogo soderzhaniia vody v myshechnykh voloknakh mlekopitaiushchikh.

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. That causes a loss of the ability of muscle fibres to restore their cell volume in the hypertonic medium.

[Effects of death of a single neuron on the functional organization of the neuronal ensemble in the leech]. / Vliianie gibeli otdel'nogo neirona na funktsional'nuiu organizatsiiu neironnoi seti meditsinskoi piiavki.

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.

[Effects of hyperosmolarity and furosemide on resting membrane potentials and skeletal muscle fiber volume in rats]. / Vliianie giperosmoliarnosti i furosemida na membrannyi potentsial pokoia i ob"em skeletnykh myshechnykh volokon krysy.

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. The hypertonic-induced decrease of the RMP was delayed in the furosemide-treated muscle. Besides, furosemide abolished the muscle fibres volume restorative properties in hypertonic medium. It is suggested that the membrane depolarisation and cell volume restoration in hypertonic medium are the resultant effects of intracellular chloride ions level elevation which, in turn, have been evoked by activation of furosemide-sensitive Cl(-)-influx system.

[The electrical and contractile activity of denervated smooth muscle]. / Elektricheskaia i sokratitel'naia aktivnost' denervirovannoi gladkoi myshtsy.

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. Spontaneous generation of the APs is only possible in denervated muscles. Pharmacomechanical type of coupling between excitation and contraction seems to be characteristic of innervated smooth muscles, whereas electromechanical type is characteristic of denervated muscles. The denervation seems to result not only in the change of cells' sensitivity to transmitters but in the abnormality of coupling processes between excitation and contraction as well.

[Simulation of the neurotrophic control of the resting membrane potential in rat skeletal muscle by using electrical stimulation and an exogenous cholinomimetic]. / Imitatsiia neirotroficheskogo kontrolia membrannogo potentsiala pokoia skeletnoi myshtsy krysy s pomoshch'iu élektricheskoi stimuliatsii i ékzogennogo kholinomimetika.

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. The resting MP in muscles with long stump of the nerve was not affected by d-tubocurarine added to the culturing medium. The action of synaptic acetylcholine via d-tubocurarine-insensitive mechanism and the nerve impulsation seem to serve as additional factors in complete actualization of the resting MP neurotrophic control.

[Role of opioid peptides in the neurotrophic control of the acetylcholine-sensitive membrane of rat skeletal muscle fibers]. / Uchastie opioidnykh peptidov v neirotroficheskom kontrole chuvstvitel'nosti k atsetilkholinu membrany skeletnykh myshechnykh volokon krysy.

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. Moreover, if this peptide was present in the culture medium in the concentration higher than that of dalargin, the effect of dalargin was blocked. It is suggested that the neurotrophic regulation of acetylcholine-sensitive membrane properties of skeletal muscle fibers is accomplished with opiate neurogenic peptide, e.g. beta-endorphin.

[Effect of acetylcholine and carbamylcholine on the resting membrane potential of denervated muscle in the rat]. / Vliianie atsetilkholina i karbamilkholina na membrannyi potentsial pokoia denervirovannoi myshtsy krysy.

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. The decrease of MP was accompanied by spontaneous release of acetylcholine for 24 hrs. Synaptic acetylcholine seems to play no obvious role in neurotrophic control of the resting MP.

[Importance of calcium ions and impulse activity for neurotrophic control of the membrane potential of muscle fibers in the rat]. / Znachenie ionov kal'tsiia i impul'snoi aktivnosti dlia neirotroficheskogo kontrolia membrannogo potentsiala myshechnykh volokon krysy.

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. The hyperpolarizing effects of carbamylcholine and electrical stimulation were not added. It is suggested that the influx of the extracellular Ca++ through acetylcholine-sensitive ionic channels in the external muscle membrane contributes to the neurotrophic regulation of the membrane potential in rat muscle fibres.

[Effect of disruption of chloride conductance on the development of denervation changes in muscle fiber membranes of the rat]. / Vliianie narusheniia khlornoi provodimosti na razvitie denervatsionnykh izmenenii membrany myshechnogo volokna krysy.

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. The Cl- are not essential in neurotrophic regulation of the electrogenic properties of membrane.

[Effect of beta-endorphin on the development of denervation changes in the membrane of the muscle fiber in the rat]. / Vliianie beta-éndorfina na razvitie denervatsionnykh izmenenii membrany myshchechnogo volokna krysy.

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. Naloxone (1.25.10(-6) M) did not avert the effect of beta-endorphin, more over it exerted a beta-endorphin-like effect on the denervated muscle fibres. It is suggested that beta-endorphin can be the factor which is responsible for the neurotrophic control of passive electrical properties of the muscle fibre membrane and neurotrophic regulation of the membrane sensitivity to acetylcholine.

[Neurotrophic control of transmembrane chlorine transport in the muscle fibers of mammals]. / Neirotroficheskii kontrol' transmembrannogo perenosa khlora v myshechnykh voloknakh mlekopitaiushchikh.

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. It is concluded that neurotrophic control disturbance leads to activation of furosemide-sensitive Cl-influx system, which causes elevation of the intracellular concentration of chloride ions and muscle membrane depolarization.

[Role of calcium ions and cyclic nucleotides in neurotrophic control of the membrane properties of muscle fibers in the frog]. / Rol' ionov kal'tsiia i tsiklicheskikh nukleotidov v neirotroficheskom kontrole svoistv membrany myshechnykh volokon liagushki.

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. The neurotrophic control of frog muscle membrane properties seems to depend on calcium and involve the cyclic nucleotides system.

[Effect of hydrocortisone on neuromuscular transmission in the frog skeletal muscles]. / Vliianie gidrokortizona na nervno-myshechnuiu peredachu v skeletnykh myshtsakh liagushki.

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.p.p., affecting neither membrane potential, nor input resistance, nor sensitivity to acetylcholine of the membrane of m. sartorius fibers. Hydrocortisone in conditions of magnesium block of neuro-muscular transmission does not affect the evoked transmission. Hydrocortisone seems to facilitate the evoked quantum acetylcholine secretion only in the presence of curare and in conditions of initial high quantum content of e.p.p. The mechanism of hydrocortisone decurarization effect on neuro-muscular transmission is mainly of a presynaptic nature.

[Effect of blockade of axonal transport on endplate currents of muscle fibers in the frog]. / Vliianie blokady aksonnogo transporta na toki kontsevoi plastinki myshechnogo volokna liagushki.

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. It is suggested that the increase in the EPC decay time constant was due to the appearance of a new population of receptor--ion channel complexes with opening time similar to that described for extrajunctional receptors after denervation. The neurotrophic control of chemosensitive muscle fibre membrane depended on the axoplasmic flow.

[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?]. / Prinimaet li uchastie nekvantovaia sekrestsiia atsetilkholina iz dvigatel'nykh nervnykh okonchanii v neirotroficheskom kontrole membrannogo potentsiala myshechnykh volokon krysy?

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. Ouabain prevented these effects. On the 5th day after the nerve section the presence of carbamylcholine or cGMP had no effect on the membrane potential. In the in vitro experiments the nonquantal acetycholine release was equal in "near" and "far" fibres and just the same as in the control preparations. A conclusion is made that synaptic acetylcholine from motor nerve endings in nonquantal form does not play a significant role in neurotrophic control of the resting membrane potential of muscle fibres membrane in mammals.

[Effect of hydrocortisone on the membrane properties of innervated and denervated muscle fibers in frogs]. / Vliianie gidrokortizona na svoistva membrany innervirovannykh i denervirovannykh myshechnykh volokon u liagushki.

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. Hydrocortisone seems to be unable to hinder the postdenervation changes in the muscle membrane whereas high doses of the hormone are able to induce changes in the muscle membrane.