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Biomedical subjects

A L Zefirov

Publications and source records attributed to A L Zefirov.

At least 37 records · Page 2Linked to original sources
PubMed2003

[Autonomic control of cardiac function involves modulation of hyperpolarization activated channels in vitro].

We examined the role of hyperpolarization-activated currents (Ih) in heart rate regulation in mongrel white rats. The ZD 7288 blocking agent decreased the heart rate. Vagus stimulation in bradycardia also decreased the heart rate and was dose-depended. Vagotomy following the ZD 7288 administration induced different dose-dependent changes in heart activity. The index figures of the heart activity following beta-AR isoproterenol administration depended on the level of hyperpolarization-activated currents. The data suggest existence of a possible modulating effect of the ANS on the hyperpolarization-activated activity of the channels.

Animals↗
PubMed2003

[Analysis of living motor nerve ending of a frog by endocytotic fluorescent marker FM 1-43].

In our experiments on motor nerve endings of the frog cutaneous pectoris muscle, using fluorescent marker FM 1-43, the intensity and topography of endocytosis were investigated after the initiation of massive exocytosis of synaptic vesicles by increasing the extracellular potassium concentration. Using FM 1-43, fluorescent spots were shown to appear, looking as accumulations of synaptic vesicles in the active zone region. The forms and sizes of luminous spots and the distances between them were analysed. Considerable variations in brightness and total areas of fluorescent spots per a length unit in different regions of the nerve ending were revealed in addition to a proximal-distal gradient of these parameters along the nerve terminal. Peculiarities of topography and intensities of luminescence in the most terminal regions of the nerve ending are described. The obtained data are discussed in terms of the exo- and endocytosis cycle of synaptic vesicles in the active zone region, and from the point of view of the plasticity of the motor nerve ending and active zones. The factors involved in the transmitter release nonuniformity are analysed.

Animals↗
PubMed2002

Blockade of hyperpolarization-activated channels modifies the effect of beta-adrenoceptor stimulation.

Experiments on rats showed that blockade of hyperpolarization-activated currents moderates tachycardia induced by beta-adrenoceptor agonist isoproterenol and potentiates the increase in stroke volume produced by this agonist. Electrical stimulation of the vagus nerve against the background of isoproterenol treatment augmented bradycardia and increased stroke volume. Blockade of hyperpolarization-activated currents followed by application of isoproterenol moderated vagus-induced bradycardia and had no effect on the dynamics of stroke volume.

Animals↗
PubMed2002

Age-related peculiarities of the effect of alpha-adrenoreceptor blockade on cardiac function in rats.

Blockade of alpha(1)-adrenoreceptors with prazosin produces bradycardia. The degree of this bradycardia in rats depends on age. In adult (20-week-old) rats bradycardia is pronounced, in 3-week-old rats it is insignificant, and in 1-week-old rats bradycardia does not develop. Prazosin moderates bradycardia induced by vagal stimulation in rats of different age.

Adrenergic alpha-Antagonists↗
PubMed2002

[Mediator secretion in the nerve-muscle synapse in the frog following long-term effect of calcium-free solutions].

The changes of spontaneous and evoked transmitter release in condition of long time (1-4 hours) incubation in Ca-free solution with EGTA adding, were investigated with extracellular recordings in experiments on the nerve-muscular junction of the frog cutaneous-pectoris muscle. Using the method of three extracellular microelectrodes recordings of the monoquantal postsynaptic signals, it was shown that during action of Ca-free solutions the topography of transmitter release changed, the specific spatial organization of points of transmitter release was disrupted. These changes remained after returning to the initial solution. The obtained data suggest that the Ca2+ free solution leads to disruption of active zones of nerve ending. In condition of low initial extracellular Ca2+ concentrations (0.15-0.4 mmol/l), the active zones disorganization led to decreasing of average amplitude of the end-plate currents (EPC) by decreasing their quantal content, increasing their time-course and decreasing the frequency of the miniature end-plate currents (MEPC). The sharp displacement of dependence of quantal contents of EPC in extracellular Ca2+ concentration to a higher Ca2+ concentration without significant changes of slope was revealed. In condition of high (1.8 mmol/l) concentration of Ca2+, the long action of Ca-free solutions leads to decreasing of amplitude of EPC too, but it was less obvious than in condition of initial low Ca2+ concentration. It is supposed that intra- and extracellular Ca concentration provides the support of the typical morpho-functional organization of the mechanisms of transmitter release at the nerve ending of the frog. The disorganization of active zones leads to separation of the elements, which take part at the transmitter release process and reduces the efficiency of secretion.

Animals↗
PubMed2002

[Pharmacological parameters of muscarinic cholinoreceptors in skeletal muscles].

It has been shown that bath application of muscarine delayed the early post-denervation depolarization in the muscle fibers incubated for 3 h in culture medium. The greatest reduction of the post-devervation depolarization was observed with 50 nmol/l muscarine. Atropine, a muscarinic antagonist, clozapine, a specific inhibitor of M1/M5-cholinergic receptors, and nitrocaramiphen, a M1-antagonist, completely removed the hyperpolarizing effect of muscarine. 4-DAMP, a specific inhibitor of M3-cholinergic receptors, himbacine, an antagonist of M2-cholinergic receptors, and tropicamide, a specific inhibitor of M2/M4-cholinergic receptors, failed to prevent the effect of muscarine. A M1/M2 muscarine agonists propargyl and but-2-ynyl esters of arecaidine had apparent muscarine-like effect. Nitrocaramiphen, and not himbacine, prevented the hyperpolarizing effect of these cholinomimetics. It is concluded that muscarine and esters of arecaidine delay the development of early postdenervation depolarization in M1-cholinergic receptors of skeletal muscle.

Acetylcholine↗
PubMed2002

[Decrease of reactivity of cerebral arteries at late stages of life].

The reactivity of cerebral arteries have been examined in three groups of patients (young, middle and adult ages). The medium meanings of the blood flow velocity (V) and the pulsativity index (Pi) were registrated in MCA and PCA under hypercapnia, hyperventilation and light stimulation. It was revealed that the reactivity of cerebral arteries in middle and especially in adult groups was decreased.

Adolescent↗
PubMed2001

Effect of exogenous nitric oxide on electrogenesis in myelinated and unmyelinated nerve fibers.

Extracellular recording was used to study the effect of sodium nitroprusside, a donor of NO, on parameters of action potential and ionic currents in single sciatic nerve fibers and unmyelinated nerve terminals in the sternal muscle in frogs. Sodium nitroprusside significantly decreased the duration of action potential in Ranvier node and the amplitude of afterdepolarization. In motor nerve terminals bathed in low Ca(2+) saline, sodium nitroprusside increased phase III amplitude of the nerve terminal response corresponding to outward potassium currents. Blockade of voltage-dependent potassium channels with 4-aminopyridine abolished the effects of NO. These data indicate that exogenous NO reduced the duration of action potential and afterdepolarization through enhancement of voltage-dependent potassium currents.

Action Potentials↗
PubMed2001

[Effect of endogenous nitric oxide on the nerve-muscle synapse function].

The nitric oxide (NO) precursor L-arginine was found to decrease the amplitude and the quantum content of the EPPs and to increase the amplitude of the AP third deflection in the frog neuromuscular junction of the m. cutaneous pectoris preparation. Inhibitor of the NO synthase NG-nitro-L-arginine methylester exerted opposite effects. The data obtained suggest that endogenous NO is produced in the neuromuscular synapse area and can modify the work of potassium ion channels.

Animals↗
PubMed1999

[Presynaptic mechanisms of zinc effects on the neuromuscular transmission].

The effect of zinc ions on presynaptic currents and transmitter release was studied at the neuromuscular junction of the frog cutaneous pectoris muscle preparation with using an extracellular microelectrode. It has been shown that zinc (100 mkM) amplified MEPP frequency at first, but suppressed it later. Zinc affected the presynaptic spike waveform and transmitter release in a concentration-dependent manner. Depending on concentration and time of exposure zinc increased or suppressed transmitter release. Increase of transmitter release was shown to be resulted by blockade voltage gated and calcium activated potassium channels in nerve ending, leading to broad of both presynaptic spike and action potential. Strong change of presynaptic spike waveform after high concentration zinc treatment supposed that under this condition zinc depressed voltage gated calcium and sodium channel leading to decrease of transmitter release. It was concluded that the final and irreversible depression of acetylcholine release by zinc was due to alteration of whole ion conductances in nerve ending and to change of configuration of proteins included in structure of ion channels. It is discussed possible mechanisms of various effects of zinc ions at the neuromuscular synapse.

Animals↗
PubMed1999

[Effect of sodium nitroprusside on the mediator release and functional properties of the postsynaptic membrane at the neuromuscular junction].

The effect of nitric oxide donor sodium nitroprusside on the end-plate currents was studied under two-electrode voltage-clamp condition at frog neuro-muscular junction. Sodium nitroprusside (10(-4) M) reduced to the half the amplitude of end-plate currents while did not change miniature end-plate currents indicating the presynaptic nature of end-plate depression. In keeping with such suggestion sodium nitroprusside essentially (to 33%) suppressed the frequency of miniature end-plate currents but did not affect the decay time constant and voltage-dependence of miniature end-plate decay. In contrast to another presynaptic inhibitors sodium nitroprusside rather reduced than increased the presynaptic facilitation and did not change postsynaptic potentials. Thus, nitric oxide is the powerful inhibitor of both evoked and spontaneous transmitter release and did not change postsynaptic potential.

Acetylcholine↗
PubMed1998

Effect of phenol on the ion currents of frog nerve ending.

The effect of phenol on the transmitter release was studied at the neuromuscular junction of a frog cutaneous pectoris muscle using the extracellular microelectrode technique. It was shown that phenol (0.5 mM) enlarged the quantal content of the end-plate currents (EPCs), and it caused the increase of duration of the second negative and third positive phases of the triphasic response observed experimentally. The amplitude of the third phase (outward K+ current) decreased, and one of the second phase was unchanged. The effect of phenol remained in the presence of the Ca(2+)-channel blockers (Co2+, Mn2+), and disappeared in the presence of the tetraethylammonium (TEA) and 4-aminopyridine (4-AP). The results suggest that phenol changes the kinetics of the voltage-dependent K+ current, which is one of the mechanisms of the phenol facilitating effect at the synaptic transmission.

Animals↗
PubMed1996

[The effect of phenol on the ion currents of the frog motor nerve ending].

Phenol was shown to enhance the quantum content of the end-plate currents and to increase the duration of the nerve ending response. The effect could be abolished by the potassium channel blockers. The data obtained suggest that alteration of the kinetics of the potential-dependent potassium current of the nerve terminal is one of the mechanisms of the phenol facilitating effect on neuro-muscular transmission.

Animals↗
PubMed1995

[The mechanisms of the recovery of nerve ending functions during the reinnervation of skeletal muscle].

At the experiments on the frog cutaneous-pectoris muscle the nerve terminal functions in course of reinnervation process were investigated by electrophysiological and morphological methods. At the 20-25th days after the nerve crushing the nerve terminal response, which reflect the nerve terminal currents, formed the propagated action potential, were restored and the arising of evoked transmitter secretion occurred. The regenerating terminals are characterized by a low amplitude and altered shape of responses, by small velocity of the excitation propagation and the low level of evoked transmitter release. The 4-aminopyridine effect at the new formed nerve terminals was quite another, than at the intact nerve terminals. This data concluded, that the membrane of regenerating nerve terminal have a low density and a small gradient of sodium channels along the terminal and have not a calcium-activated potassium channels. It was proposed, that different kinds of channels are inserted into the nerve endings membrane at the different periods of the reinnervation process.

4-Aminopyridine↗
PubMed1994

The effect of acetylcholine and related drugs on currents at the frog motor nerve terminal.

Acetylcholine, acetylthiocholine, carbachol, suberyldicholine, propionylcholine, succinylcholine, methylfurmethide and F 2268 were tested on motor nerve ending currents recorded with an extracellular microelectrode. The isolated and transversally cut cutaneous pectoris muscle of frog Rana ridibunda was used. Only acetylcholine and acetylthiocholine affected the spike waveforms in a concentration-dependent manner. Lower concentrations (1-6 x 10(-4) M) prolonged the inward Na+ current and increased the outward K+ current at the proximal and central parts of the nerve terminal. Most remote parts of the terminal were not affected. At 7 x 10(-4) M and higher, both drugs further prolonged the Na+ current and eliminated the K+ component of the spike. The potentiating effect of acetylcholine and acetylthiocholine on the K+ phase of nerve terminal current disappeared after treatment with tetraethylammonium and 4-aminopyridine. The effect also disappeared when synaptic cholinesterase was inhibited by the anticholinesterases or by treatment with collagenase. Reactivation of cholinesterase by dipyroxime restored the facilitating effect of acetylcholine. Choline and slight acidification to pH 6.8 did not mimic the acetylcholine action on the terminal currents. Facilitation of the K+ current by acetylcholine was not calcium-dependent. The results indicate that lower acetylcholine concentrations inhibit the delayed rectifier only, whereas 7 x 10(-4) M and higher concentrations of acetylcholine depress all outward currents of the terminal.

Acetylcholine↗