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1.
Bull Exp Biol Med ; 150(3): 295-8, 2011 Jan.
Article in English | MEDLINE | ID: mdl-21240338

ABSTRACT

We studied possible involvement of ATP in the influence of protein sensitization on contractile function and non-quantum secretion in the end-plate of isolated skeletal muscles from mouse leg. The dynamic vector of muscle contraction force was shown to correlate with changes in non-quantum secretion of acetylcholine under various conditions of experimental pathology. However, the degree of these changes was lower in sensitized animals. It can be hypothesized that the ATP-induced variability in functional properties of slow muscles during protein sensitization reflects the development of resistance to external loads. The adaptive changes in fast muscles during protein sensitization are not associated with the ATP-mediated mechanisms of excitation.


Subject(s)
Acetylcholine/metabolism , Adenosine Triphosphate/pharmacology , Muscle Contraction/drug effects , Muscle, Skeletal/physiology , Adenosine Triphosphate/metabolism , Animals , Biomechanical Phenomena , Mice , Muscle Contraction/physiology
2.
Bull Exp Biol Med ; 151(3): 280-3, 2011 Jul.
Article in English, Russian | MEDLINE | ID: mdl-22451866

ABSTRACT

Experiments in vitro showed that ATP and adenosine equally suppressed contractions of frog m. sartorius, which belongs to the phasic type muscles. Adenosine receptors antagonist 8-SPT abolished the effect of adenosine, but did not change the effect of ATP. This fact proves the independence of signaling pathways of these purines. ATP produced an opposite effect on the tonic muscle m. cruralis and increased the force of its contraction. Adenosine produced an inhibitory effect on the force of m. cruralis contration. In this case, 8-SPT also eliminated the effect of adenosine, but did not change the effect of ATP. The potentiating effect of ATP was blocked by suramin, a nonselective antagonist of P2 receptors, which attests to their involvement into the effects of this purine. The opposite effects of purinergic regulation reflect fundamental differences in functional organization of phasic and tonic muscular systems. It was hypothesized that the increase in contraction force under the effect of ATP is a mechanism providing maitenance of the contracted state of tonic muscle without appreciable metabolic costs.


Subject(s)
Adenosine Triphosphate/metabolism , Adenosine/metabolism , Muscle Contraction/drug effects , Muscle, Skeletal/metabolism , Muscle, Skeletal/physiology , Adenosine/pharmacology , Adenosine Triphosphate/pharmacology , Animals , Calcium/metabolism , Muscle Contraction/physiology , Muscle Fibers, Skeletal/drug effects , Muscle Fibers, Skeletal/metabolism , Muscle Fibers, Skeletal/physiology , Muscle, Skeletal/drug effects , Rana ridibunda , Receptors, Purinergic P1/metabolism , Signal Transduction , Suramin/pharmacology , Theophylline/analogs & derivatives , Theophylline/pharmacology
3.
Bull Exp Biol Med ; 147(5): 560-3, 2009 May.
Article in English, Russian | MEDLINE | ID: mdl-19907738

ABSTRACT

We studied the mechanisms underlying the effect of immunobiological reorganization of the organism on contractile function of isolated skeletal muscles from mouse leg (fast muscle, m. extensor digitorum longus; and slow muscle, m. soleus). Protein sensitization was accompanied by changes in contractile properties of fast and slow skeletal muscles. These changes were differently directed in muscles with various phenotypes. The force of carbachol-induced contraction (cholinergic agonist) increased in the slow muscle, but decreased in the fast muscle. The direction of changes in the force of carbachol-induced contractions under conditions of protein sensitization in skeletal muscles correlates with changes in non-quantal secretion of acetylcholine in the endplate (H-effect). Opposite changes in functional properties of fast and slow muscles from mouse leg during protein sensitization are related to choline-mediated excitation of the muscle fiber membrane. Our results suggest that changes in contractile function of skeletal muscles during protein sensitization are associated with variations in choline-mediated excitation of the muscle fiber membrane and modification of electromechanical coupling.


Subject(s)
Muscle Fibers, Fast-Twitch/metabolism , Muscle Fibers, Slow-Twitch/metabolism , Muscle, Skeletal/drug effects , Muscle, Skeletal/physiology , Aluminum Hydroxide/pharmacology , Animals , Carbachol/pharmacology , Female , Male , Mice , Muscle Contraction/drug effects , Muscle Contraction/physiology , Muscle Fibers, Fast-Twitch/drug effects , Muscle Fibers, Slow-Twitch/drug effects , Muscle, Skeletal/metabolism , Ovalbumin/pharmacology
4.
Bull Exp Biol Med ; 141(5): 633-5, 2006 May.
Article in English | MEDLINE | ID: mdl-17181071

ABSTRACT

GABA, baclofen, epinephrine, and norepinephrine hyperpolarized the membrane of earthworm somatic cells. This effect was prevented by furosemide, removal of Cl- from the medium, or activation of Na+/K+ pump by 3-fold increase external potassium concentration. It was hypothesized that GABA, baclofen, epinephrine, and norepinephrine stimulate Na+/K+ transport via specific receptor inputs, but their effect on resting potential can be realized only under conditions of working Cl- symport.


Subject(s)
Adrenergic Agents/pharmacology , GABA Agents/pharmacology , Membrane Potentials/drug effects , Muscles/drug effects , Oligochaeta/metabolism , Sodium Chloride Symporters/metabolism , Sodium-Potassium-Exchanging ATPase/metabolism , Animals , Muscles/metabolism
5.
Bull Exp Biol Med ; 141(4): 407-9, 2006 Apr.
Article in English | MEDLINE | ID: mdl-17152356

ABSTRACT

We studied the effects of adenosine and ATP on contractile function of the isolated strip from mouse diaphragm. ATP significantly increased the strength of muscle contraction induced by carbachol. Adenosine had no effect on carbachol-induced muscle contraction. P2 receptor antagonist suramin abolished the effect of ATP. The positive chronotropic effect of ATP was not observed after treatment with specific protein kinase C inhibitor chelerythrine. Our results indicate that the effect of ATP on contractile function of mouse diaphragm is realized via protein kinase C.


Subject(s)
Adenosine Triphosphate/metabolism , Diaphragm/enzymology , Muscle Contraction/physiology , Muscles/enzymology , Protein Kinase C/physiology , Adenosine/pharmacology , Alkaloids/metabolism , Animals , Benzophenanthridines/metabolism , Carbachol/pharmacology , Cardiotonic Agents/pharmacology , Diaphragm/metabolism , Female , Male , Mice , Protein Kinase C/metabolism , Suramin/pharmacology , Vasodilator Agents/pharmacology
6.
Bull Exp Biol Med ; 141(3): 278-80, 2006 Mar.
Article in English | MEDLINE | ID: mdl-17073138

ABSTRACT

We studied parameters of the frog sartorius muscle contraction initiated by ryanodine receptor agonists in the presence of ROS donors. We hypothesized that sodium nitroprusside and hydrogen peroxide inhibit initiation of contractions by N-ethylmaleimide and that this effect of ROS donors on parameters of N-ethylmaleimide-induced contractions is due to a direct effects of sodium nitroprusside and hydrogen peroxide on N-ethylmaleimide, but not to inactivation of ryanodine receptors in the sarcoplasmatic reticulum of frog skeletal muscle.


Subject(s)
Ethylmaleimide/pharmacology , Muscle Contraction/drug effects , Animals , Ranidae , Reactive Oxygen Species/metabolism , Ryanodine Receptor Calcium Release Channel/drug effects
7.
Neurosci Behav Physiol ; 36(3): 307-12, 2006 Mar.
Article in English | MEDLINE | ID: mdl-16465498

ABSTRACT

Arachidonic acid and prostaglandin E2 decreased the frequency of miniature endplate potentials with producing any changes in the their amplitude-time parameters. Arachidonic acid and prostaglandin E2 decreased the quantum composition of endplate currents and the amplitude of the third phase of the nerve ending response, which reflects currents though potential-dependent K+ channels. A perineural method was used to demonstrate that arachidonic acid and prostaglandin E2 suppressed the nerve ending Ca2+ current. The cyclooxygenase blocker indomethacin increased neurotransmitter secretion and decreased the third phase of the nerve ending response. The effects of arachidonic acid and prostaglandin E2 on evoked neurotransmitter release were not seen in the presence of indomethacin, while the third phase of the response continued to show a reduction. It is suggested that prostaglandin E2 mediates the effects of arachidonic acid on spontaneous and evoked neurotransmitter secretion, Ca2+ currents, and Ca2+ -dependent K+ currents. In addition, arachidonic acid and prostaglandin E2 had their own effects on potential-dependent K+ currents in nerve endings.


Subject(s)
Arachidonic Acid/physiology , Dinoprostone/physiology , Neuromuscular Junction/physiology , Synapses/physiology , Animals , Arachidonic Acid/pharmacology , Calcium/physiology , Cyclooxygenase Inhibitors/pharmacology , Dinoprostone/pharmacology , In Vitro Techniques , Indomethacin/pharmacology , Motor Endplate/physiology , Neuromuscular Junction/drug effects , Potassium Channels/physiology , Rana ridibunda
9.
Bull Exp Biol Med ; 139(2): 249-51, 2005 Feb.
Article in English, Russian | MEDLINE | ID: mdl-16027820

ABSTRACT

GABA, baclofen, isoguvacine increase, and cis-4-aminocrotonic acid does not modify resting membrane potential of muscle cells. Bicuculline, phaclofen, N-ethylmaleimide, chlorpromazine, verapamil, and removal of Ca2+ from bathing solution abolished the effect of baclofen, while U73122 and D609 were ineffective in this respect. The authors conclude that the Lumbricus terrestris muscle cells contain GABAergic structures similar to a- and b-receptors. Activation of GABA receptors induced Cl- inward current and Ca2+ entry with subsequent activation of calmodulin-like proteins, which causes membrane hyperpolarization by increasing the effect of "pumping potential" on resting membrane potential.


Subject(s)
Muscle Cells/physiology , Oligochaeta/physiology , Receptors, GABA/physiology , gamma-Aminobutyric Acid/pharmacology , Animals , Cell Membrane/drug effects , Cell Membrane/physiology , GABA Agonists/pharmacology , GABA Antagonists/pharmacology , Membrane Potentials/drug effects , Muscle Cells/drug effects , Muscles/cytology , Oligochaeta/drug effects , Receptors, GABA/drug effects
10.
Ross Fiziol Zh Im I M Sechenova ; 91(3): 268-76, 2005 Mar.
Article in Russian | MEDLINE | ID: mdl-15881878

ABSTRACT

Arachidonic acid and prostaglandin E2 decreased the frequency of miniature endplate currents without changing their amplitude-temporary parameters. They also reduced the evoked transmitter release and the amplitude of the 3rd phase of nerve ending response corresponding to the voltage-dependent K(+)-current. Using perineural recording, It was shown that arachidonic acid and prostaglandin E2 decreased the Ca2+ currents of nerve endings. Indometacin: inhibitor of cyclooxygenase, enhanced the evoked transmitter release and decreased the 3rd phase of nerve ending response. Indometacin prevented the effects of arachidonic acid on evoked transmitter release, whereas the effects of arachidonic acid on the 3rd phase was preserved. Prostaglandin E2 seems to mediate the effects of arachidonic acid on spontaneous and evoked transmitter release, Ca(2+)- and Ca(2+)-activated K(+)-currents. Moreover, the arachidonic acid and prostaglandin E2 exerted their own effects upon voltage-dependent potassium current of motor nerve ending.


Subject(s)
Arachidonic Acid/physiology , Dinoprostone/physiology , Neuromuscular Junction/physiology , Potassium Channels, Voltage-Gated/physiology , Presynaptic Terminals/physiology , Acetylcholine/metabolism , Action Potentials , Animals , Arachidonic Acid/pharmacology , Calcium/physiology , Cyclooxygenase Inhibitors/pharmacology , Dinoprostone/pharmacology , Electrophysiology , In Vitro Techniques , Indomethacin/pharmacology , Motor Endplate/drug effects , Motor Endplate/physiology , Muscle, Skeletal/innervation , Neuromuscular Junction/drug effects , Potassium Channels/physiology , Presynaptic Terminals/drug effects , Rana ridibunda
11.
J Physiol ; 565(Pt 1): 229-42, 2005 May 15.
Article in English | MEDLINE | ID: mdl-15774519

ABSTRACT

During normal cell metabolism the production of intracellular ATP is associated with the generation of reactive oxygen species (ROS), which appear to be important signalling molecules. Both ATP and ROS can be released extracellularly by skeletal muscle during intense activity. Using voltage clamp recording combined with imaging and biochemical assay of ROS, we tested the hypothesis that at the neuromuscular junction extracellular ATP generates ROS to inhibit transmitter release from motor nerve endings. We found that ATP produced the presynaptic inhibitory action on multiquantal end-plate currents. The inhibitory action of ATP (but not that of adenosine) was significantly reduced by several antioxidants or extracellular catalase, which breaks down H2O2. Consistent with these data, the depressant effect of ATP was dramatically potentiated by the pro-oxidant Fe2+. Exogenous H2O2 reproduced the depressant effects of ATP and showed similar sensitivity to anti- and pro-oxidants. While NO also inhibited synaptic transmission, inhibitors of the NO-producing cascade did not prevent the depressant action of ATP. The ferrous oxidation in xylenol orange assay showed the increase of ROS production by ATP and 2-MeSADP but not by adenosine. Suramin, a non-selective antagonist of P2 receptors, and pertussis toxin prevented the action of ATP on ROS production. Likewise, imaging with the ROS-sensitive dye carboxy-2',7'-dichlorodihydrofluorescein revealed increased production of ROS in the muscle treated with ATP or ADP while UTP or adenosine had no effect. Thus, generation of ROS contributed to the ATP-mediated negative feedback mechanism controlling quantal secretion of ACh from the motor nerve endings.


Subject(s)
Acetylcholine/metabolism , Adenosine Triphosphate/metabolism , Motor Neurons/physiology , Neuromuscular Junction/metabolism , Presynaptic Terminals/metabolism , Reactive Oxygen Species/metabolism , Synaptic Transmission/physiology , Animals , Extracellular Fluid/metabolism , Membrane Potentials/physiology , Motor Endplate/physiology , Neural Inhibition/physiology , Rana ridibunda
12.
Bull Exp Biol Med ; 136(2): 189-91, 2003 Aug.
Article in English | MEDLINE | ID: mdl-14631507

ABSTRACT

Serotonin, glutamate, glycine, ATP, and muscarine had no effect on resting membrane potential of muscle cell in earthworm Lumbricus terrestris. Nicotine depolarizes and GABA hyperpolarizes the muscle membrane. Removal of K(+), Cl(-) and addition of ouabaine and strychnine to the solution abolished the effect of GABA. The authors conclude that the Lumbricus terrestris myocyte membrane contains nicotine receptors and GABAergic receptors sensitive to strychnine. Stimulation of these receptors activates sarcolemmal ionic pumps and causes membrane hyperpolarization.


Subject(s)
Cell Membrane/drug effects , Membrane Potentials/physiology , Neurotransmitter Agents/pharmacology , Oligochaeta/anatomy & histology , Animals , Biological Transport/physiology , Cell Membrane/metabolism , Chlorides/metabolism , Convulsants/pharmacology , Dose-Response Relationship, Drug , Muscles/cytology , Muscles/drug effects , Muscles/metabolism , Neurotransmitter Agents/metabolism , Oligochaeta/metabolism , Potassium/metabolism , Strychnine/pharmacology
13.
Neurosci Behav Physiol ; 32(6): 589-93, 2002.
Article in English | MEDLINE | ID: mdl-12469885

ABSTRACT

Cholinomimetics not only activate postsynaptic cholinoreceptors in neuromuscular synapses, but also alter the process of acetylcholine secretion from nerve endings. However, the mechanism of action of cholinomimetics on the secretory process remains unidentified. We approached the question of the mechanism of the presynaptic action of cholinomimetics in the present study by investigating the effects of the n,m-cholinomimetic carbachol on nerve ending currents and postsynaptic membrane currents. Carbachol induced decreases in the postsynaptic response, without affecting the duration and amplitude of the nerve ending current in both the central and distal part of the nerve ending. However, carbachol increased the time between the arrival of the presynaptic action potential and the start of transmitter secretion. This effect on synaptic delay was more marked in the distal parts of the ending. The action of another potential modulator, extracellular potassium, was accompanied by decreases in presynaptic currents and also by increases in synaptic delay. These data provide evidence for the suppressive effect of carbachol on acetylcholine secretion acting via presynaptic metabotropic cholinoreceptors which control the level and time course of secretion of neurotransmitter quanta.


Subject(s)
Carbachol/pharmacology , Motor Neurons/drug effects , Nerve Endings/drug effects , Parasympathomimetics/pharmacology , Acetylcholine/metabolism , Action Potentials/drug effects , Animals , Anura , Depression, Chemical , Excitatory Postsynaptic Potentials/drug effects , In Vitro Techniques , Motor Neurons/metabolism , Muscle, Skeletal/innervation , Nerve Endings/metabolism , Neuromuscular Junction/drug effects , Neuromuscular Junction/metabolism , Potassium/pharmacology , Receptors, Presynaptic/drug effects
14.
Ross Fiziol Zh Im I M Sechenova ; 87(4): 507-13, 2001 Apr.
Article in Russian | MEDLINE | ID: mdl-11449978

ABSTRACT

Carbacholine depressed postsynaptic currents in the frog m. sartorius leaving intact presynaptic currents in proximal and distal portions of the motor nerve ending. The carbacholine depressing action was followed by an increase in the time gap between the beginning of presynaptic depolarisation and subsequent quantal release. This effect was considerably more obvious in the distal portions of the nerve endings. Effect of extracellular potassium was evident in a diminishing of presynaptic currents due to membrane depolarisation. The data obtained suggest that carbacholine presynaptically depresses synaptic transmission via metabotropic cholinergic receptors controlling the time course of the transmitter release.


Subject(s)
Carbachol/pharmacology , Cholinergic Agents/pharmacology , Cholinergic Agonists/pharmacology , Nerve Endings/physiology , Animals , In Vitro Techniques , Nerve Endings/drug effects , Potassium/metabolism , Rana ridibunda , Synapses/drug effects , Synapses/physiology
15.
Eur J Neurosci ; 13(11): 2047-53, 2001 Jun.
Article in English | MEDLINE | ID: mdl-11422445

ABSTRACT

The postsynaptic membrane of the neuromuscular synapse treated with antiacetylcholinesterase is depolarized due to nonquantal release of acetylcholine (ACh) from the motor nerve ending. This can be demonstrated by the hyperpolarization produced by the application of curare (H-effect). ATP (1 x 10-5 M) decreased the magnitude of the H-effect from 5 to 1.5 mV. The membrane input resistance and the ACh sensitivity were unchanged, and so changes in these cannot explain the ATP effect. Adenosine alone was without effect on the nonquantal release. On the other hand, both ATP and adenosine depressed the frequency of spontaneous miniature endplate potentials, to 56% and 43% respectively. The protein kinase A inhibitor Rp-cAMP or the guanylyl cyclase inhibitor 1H-[1,2,4]oxidiazolo[4,3-a]quinoxalin-1-one did not affect the inhibitory influence of ATP on the H-effect, whereas staurosporine, an inhibitor of protein kinase C, completely abolished the action of ATP. Suramin, an ATP antagonist, enhanced the H-effect to 8.6 mV and, like staurosporine, prevented the inhibitory effect of ATP. ATP thus suppresses the nonquantal release via a direct action on presynaptic metabotropic P2 receptors coupled to protein kinase C, whilst adenosine exerts its action mainly by affecting the mechanisms underlying quantal release. These data, together with earlier evidence, show that nonquantal release of ACh can be modulated by several distinct regulatory pathways, in particular by endogenous substances which may or may not be present in the synaptic cleft at rest or during activity.


Subject(s)
Acetylcholine/metabolism , Adenosine Triphosphate/metabolism , Adenosine/metabolism , Neuromuscular Junction/metabolism , Synaptic Membranes/metabolism , Synaptic Transmission/physiology , Synaptic Vesicles/metabolism , Adenosine/pharmacology , Adenosine Triphosphate/pharmacology , Animals , Antineoplastic Agents/pharmacology , Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors , Cyclic AMP-Dependent Protein Kinases/metabolism , Enzyme Inhibitors/pharmacology , Guanylate Cyclase/antagonists & inhibitors , Guanylate Cyclase/metabolism , Male , Membrane Potentials/drug effects , Membrane Potentials/physiology , Mice , Muscle, Skeletal/drug effects , Muscle, Skeletal/innervation , Muscle, Skeletal/metabolism , Neuromuscular Junction/drug effects , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide Synthase/metabolism , Rats , Rats, Wistar , Suramin/pharmacology , Synaptic Membranes/drug effects , Synaptic Transmission/drug effects , Synaptic Vesicles/drug effects
16.
Ross Fiziol Zh Im I M Sechenova ; 86(10): 1293-9, 2000 Oct.
Article in Russian | MEDLINE | ID: mdl-11200330

ABSTRACT

Daily administration of hydrocortisone first increased and then decreased amplitude of multiquantal end-plate currents induced by motor nerve stimulation. The initial facilitating phase of the hormone action was accompanied by elimination of the ATP pre-synaptic effect. Later the inhibitory effect of the ATP becomes restored. The counteraction of the ATP effect was reproduced in the isolated muscle bathed in the saline with hydrocortisone which suggests a non-genomic action of the hormone on pre-synaptic P2 receptor. The data obtained suggest that prevention of the ATP inhibitory action might be a component of a facilitating acute stress reaction.


Subject(s)
Adenosine Triphosphate/pharmacology , Adenosine/pharmacology , Hydrocortisone/pharmacology , Neuromuscular Junction/drug effects , Adenosine/physiology , Adenosine Triphosphate/physiology , Animals , Hydrocortisone/physiology , In Vitro Techniques , Membrane Potentials , Motor Endplate/drug effects , Motor Endplate/physiology , Muscle, Skeletal/innervation , Neuromuscular Junction/physiology , Rana ridibunda , Sciatic Nerve/physiology , Synapses/drug effects , Synapses/physiology
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