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Biomedical subjects

D P Matiushkin

Publications and source records attributed to D P Matiushkin.

At least 19 recordsLinked to original sources
PubMed1999

[Modulatory effects of various factors of muscular origin on the function of the motor nerve endings].

Muscle incubate was shown to contain factors capable to increase the transmitter release in low-effective synapses and decrease it in high-effective those, dueto activation and inhibition, respectively, of the processes governing formation of available store of the transmitter. Activatiory effect of the low-molecular fraction on the low-effective synapses was correlated with the concentration of histidine-containing substances in this fraction.

Animals↗
PubMed1992

[The possible function of Schwann cells in neuromuscular transmission in the frog].

Anti-galactoside rabbit antisera increased the frequency of slow (atypical) MEPPs. No lysis of the Schwann cells was found in synaptic regions. The data obtained suggest that fixation of antibodies to galactocerebroside on the Schwann cell surface membrane alters the cell's activity thus affecting some characteristics of neuromuscular transmission.

Animals↗
PubMed1989

[Effect of antibodies to glial glycolipid antigens on miniature end-plate potentials].

Less than 4% of miniature end-plate potentials (MEPPs) in frog cutaneous-pectoral muscles, normal or exposed to nonimmune rabbit serum were atypical. These MEPPs were of normal amplitude, but their time course was nearly twice as slow as that of normal MEPPs. The exposure of muscles to rabbit anti-galactocerebroside serum induced more than three-fold increase in the fraction of atypically slow MEPPs. Inhibition of acetylcholinesterase caused an appearance of giant MEPPs, the fraction of slow MEPPs being unchanged. Possible mechanisms of increase in fraction of atypical slow MEPPs based on modification of the synaptic Schwann cell functioning are discussed.

Acetylcholinesterase↗
PubMed1988

[Effect of hyaluronidase on the end-plate miniature currents and potentials in the frog].

The effect of 0.1% hyaluronidase on miniature end-plate potentials and currents (MEPP and MEPC) was studied in the frog cutaneous-pectoris muscle. The action of hyaluronidase on armin-pretreated muscles caused a decrease in the amplitude, duration of half-decay time and rising phase of MEPPs and MEPCs. The positive correlation between the amplitude and half-decay time of MEPPs and MEPCs was diminished. Hyaluronidase treatment of preparations with active acetylcholinesterase caused the half-life time of MEPCs to increase without any changes in the amplitude and rising phase of MEPCs. It is suggested that enzymatic destruction of a part of the glycocalix of cells forming the neuromuscular junction and of a part of the extracellular matrix results in a weakening of the nonspecific acetylcholine binding, thus facilitating the acetylcholine diffusion into the synaptic cleft.

Animals↗
PubMed1988

[Biochemical characteristics of a muscle perfusate and its effects on mediator release in the neuromuscular synapse].

Histidine-containing compounds (HCC) were found, using diazoreaction and reaction with diethylpyrocarbonate, a specific histidine reagent, in the perfusate of the frog hindlimb vasculature. After gel filtration on sephadex G-25 about 80% of HCC were eluted with a fraction with molecular mass less than 5000 kD. The studies of the perfusate influence on the characteristics of quantum secretion of transmitter in the preparation of frog cutaneopectoral muscle have shown that the perfusate increased the quantum content of end-plate potentials (EPP) due to increasing binominal parameter and decreasing frequency of miniature EPP. The characteristics of presynaptic action of the perfusate were similar to those of exogenous histidine.

Animals↗
PubMed1986

[Paradoxical reactions of a neuromuscular preparation (on the 100th anniversary of their discovery by N.E. Vvedenskii)].

The discovery of the intensity of repetitive stimulation pessimum and of the paradoxical response to stregthening of stimuli in a parabiotic nerve, is presented in historical aspect. Both phenomena are shown to be based on the mutual electrical delay in propagated APs when the number of synchronously activated nerve fibers is increased. The delay may cause a propagation block through these nerve regions where the safety factor is diminished.

Action Potentials↗
PubMed1986

[Release of beta-alanine from the frog skeletal muscle determined by thin-layer chromatography].

The release of beta-alanine from the resting and contracting frog sartorius muscles was demonstrated by the two-dimensional thin-layer chromatography. The release of beta-alanine from indirectly stimulated muscles of frogs in winter was about 230% higher than at rest. When synaptic transmission was blocked by d-tubocurarine the release of beta-alanine from directly stimulated muscles did not exceed the release at rest. Thus, activation of neuromuscular synapse leads to increased beta-alanine release from contracting muscle.

Alanine↗
PubMed1985

[Miniature currents of the endplates of the muscle fibers of the diaphragm of the rat after inhibition of acetylcholinesterase with galanthamine].

Miniature end-plate currents (MEPC) in rat diaphragm were studied with voltage-clamp technique when synaptic acetylcholinesterase (AChE) was inhibited with different concentrations of galanthamine. The MEPC amplitude and time course were increased progressively with galanthamine concentrations in the range of 3.16 X 10(-8) - 10(-6) g/ml. The decay of MEPC was always exponential. The input resistance of muscle fibres increased. Galanthamine (10(-5) g/ml) produced a curare-like action: the amplitude and duration of MEPC were less as compared with those at galanthamine concentration 10(-6) g/ml, the decay of MEPC became biphasic. During washing out of the drug, the duration of MEPC began to increase and then to diminish, returning to the initial value 3 hours later. The decay of MEPC became exponential. A positive correlation was found between half-decay time and amplitude of MEPC both in the presence and in the absence of anticholinesterase. It is supposed that the functional role of synaptic AChE in limiting the postsynaptic effect of acetylcholine is not so significant as it is usually considered, therefore it is possible to use the parameters of MEPC for the estimation of functional AChE activity.

Acetylcholinesterase↗
PubMed1984

[Sodium and potassium content of intrafusal muscle fibers and their resting membrane potential in different ionic media].

X-ray microanalysis revealed a high sodium concentration in intrafusal fibers of the frog-muscle whereas it appeared to be normal in extrafusal ones. Potassium concentration was practically the same both in intra- and extrafusal fibers which is in good agreement with the data obtained earlier with other techniques. Electrophysiological experiments demonstrated a similar behaviour of the resting MP found in both kinds of fibers in solutions with different ionic composition. The concentration of free sodium ions seems to be the same in intra- and extrafusal muscle fibers. The intrafusal fibers have believed to suggest a high amount of immobilized sodium.

Animals↗
PubMed1984

[Antidromic action of potassium in the neuromotor synapse].

The possibility of potassium accumulation in the synaptic cleft and a participation of its antidromic action in the regulation of presynaptic processes were estimated in experiments on neuromuscular junctions of the frog. In potassium-enriched solution, the reversal potential obtained by the linear extrapolation from the region of high membrane potentials was considerably altered according to the Takeuchi equation. The change of the reversal potential obtained by interpolation was insignificant as predicted by the Goldman--Hodgkin--Katz equation. In normal solution under the change of the nerve stimulation frequency from 0.5/sec to 50/sec the positive shift of the reversal potential occurred as revealed by both techniques. This indicates potassium accumulation in active synaptic segments during the activity. Elimination of the potassium component in the end-plate current by clamping of the membrane potential at the -130 mV level resulted in lowering of facilitation under paired nerve stimulation (20 msec interval) and in a decrease of the facilitation rate under 50/sec stimulation. The data corroborate an antidromic potassium action on the neuromuscular synapse.

Animals↗
PubMed1984

[Analysis of the paradoxical stage of neural cathodal parabiosis (the reciprocal inhibition of adjacent fibers)].

A preparation consisting of VIII-IX dorsal and ventral roots, the sciatic nerve and a single fiber of the tibial nerve was used to study changes in conduction reliability in a single nerve fiber by means of steady-state depolarization ("cathodal alteration") of the central part of the sciatic nerve: the depolarization led to a partial block of nerve fibers and to lowering of the safety factor in the single fiber tested. While a spinal root containing the fiber under study was stimulated with trains of stimuli (200/s) the number of APs traveling along the fiber depended on the stimulation strength, being maximal near the threshold. This suggests the influence of neighbouring fiber excitation on the conduction in the tested one. The effect was more obvious when all four roots were stimulated. The paradoxical decrease in the conducted APs caused by intensification of the stimulation, seems to reflect the electrical interaction between activated fibers. Possible mechanism of this interaction is discussed.

Action Potentials↗
PubMed1983

[Presynaptic action of armin and galantamin on mammalian neuromuscular junction].

Actions of the two cholinesterase inhibitors: armin and galanthaamine on the neuromuscular transmission and on the spontaneous and evoked acetylcholine release were studied in the rat diaphragm. High concentrations (greater than or equal to 10(-6) g/ml) of these agents exhausted the available transmitter store which decreased the quantum content of e. p. p. sin single nerve stimulation. At the repetitive stimulation (10-100 s-1), armin and galanthaamine accelerated the presynaptic depression of e. p. p. s and slowed down the rate of transmitter mobilization. This resulted in a rapid decrease of quantum content and amplitude of e. p. p. s. The found presynaptic deteriorations together with the stationary postsynaptic depolarization may cause the neuromuscular block.

Action Potentials↗