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O D Uchitel

Publications and source records attributed to O D Uchitel.

54 records · Page 3Linked to original sources
PubMed1987

Characteristics of synaptic currents in frog muscle fibers of different types.

A study was made of synaptic currents in voltage-clamped muscle fibers of the frog. Fast, submaxillaris, and slow muscle fibers are innervated by nerve fibers of different conduction velocities. To avoid spatial complications, transmitter release by nerve impulses was restricted to the site of recording and reduced to single quanta (unitary endplate currents: uepc). Following nerve stimulation, the time course of transmitter release was longer and more variable in slow and submaxillaris muscle fibers than in the fast fibers. The time constant of decay of uepc in submaxillaris and slow fibers was, respectively, about 1.8 and 2.9 times slower than the decay of uepc in fast fibers. This is due mainly to differences in the lifetime of the channels opened by acetylcholine. The neuromuscular junctions in submaxillaris muscle fibers are bouton-like or longer branched contacts; and the unitary currents in the bouton junctions have a slower time course. It is concluded that the synaptic membrane in the different types of muscle fibers has synaptic acetylcholine-operated channels that have different kinetic properties, and that these properties are determined by the type of axon that innervates the muscle fiber.

Animals↗
PubMed1986

Electrophysiologic denervation changes of human muscle fibers in motoneuron diseases.

Muscle denervation and reinnervation by sprouting of the surviving motoneurons characterizes motoneuron diseases (MND). In mammalian muscles, experimental denervation induces the appearance of extrajunctional acetylcholine (ACh) receptors and tetrodotoxin (TTX) resistant action potentials (AP). These denervation changes have been investigated in muscle biopsies from 10 MND patients and in 2 traumatically denervated normal human muscles. Extrajunctional ACh sensitivity was present in 113 of the 140 (73%) fibers from MND muscles studied. In 50 of 84 (70%) ACh-sensitive fibers, no TTX-resistant AP were present. The remaining fibers (30%) showed small regenerative responses. In contrast, all the traumatically denervated muscle fibers showed extrajunctional ACh sensitivity and TTX-resistant AP. Histochemical analysis of the biopsies showed no direct correlation between the frequency of ACh-sensitive fibers and that of the atrophic or normal-appearing fibers. The absence of TTX-resistant AP in ACh-sensitive fibers and its lack of correlation with the histochemical criteria of denervation suggest the presence of a state of innervation in MMD, where the motoneuron is not able to maintain its fully trophic influence on the muscle fiber membrane.

Acetylcholine↗
PubMed1984

Characteristics of membrane channels induced by acetylcholine at frog muscle-tendon junctions.

The membrane at the tendinous ends of frog muscle fibres has acetylcholine (ACh) receptors that are blocked by alpha-bungarotoxin. The properties of ACh-activated channels in the myotendinous region were investigated by noise analysis. These channels displayed the same characteristics in normal, denervated and reinnervated muscles. The mean lifetime and conductance of ACh-induced channels at the myotendinous junction resembled those of channels at the normal neuromuscular junction. Both channels opened with a lifetime shorter than that of extrajunctional receptors. Channels of short lifetime could be detected at distances of several hundred micrometres from the tendon junction. The similarity of ACh-activated channels at neuromuscular and myotendon junctions was found both in the fast, 'singly' innervated sartorius and cutaneous pectoris muscle and in the intermediate, multiply innervated submaxillaris muscle.

Acetylcholine↗
PubMed1984

A study of the submaxillaris muscle of the frog.

The characteristics of muscle fibres in the submaxillaris muscle of the frog were studied using electrophysiological and anatomical techniques. The muscle fibres were capable of eliciting action potentials and their passive membrane properties were similar to those of fast muscle fibres. Composite end-plate potentials, due to polyneuronal innervation, were observed in most muscle fibres. Acetylcholinesterase staining of the whole muscle revealed multiple end-plate areas, and several end-plates of different size and shape were observed in single teased fibres. It is concluded that the submaxillaris muscle of the frog is composed of a distinctive population of muscle fibres (intermediate muscle fibres) with electrical properties like those of fast muscle fibres and multiple innervation like that of slow muscle fibres.

Action Potentials↗
PubMed1982

Denervation changes in normal and myasthenia gravis human muscle fibres during organ culture.

1. Human intercostal nerve-muscle obtained from normal and myasthenia gravis affected patients has been organ cultured for up to 5 weeks at 23 degrees C. In addition normal nerve-muscle has been cultured for up to 2 weeks at 36 degrees C. Muscle fibres had normal resting and overshooting action potentials. Input resistances dropped markedly after 21 days at 23 degrees C or 10 days at 36 degrees C.2. Muscle fibre action potentials became partially resistant to tetrodotoxin (10(-7) g/ml.) after culturing for 8 days at 36 degrees C.3. Extrajunctional acetylcholine (ACh) sensitivity was compared in fresh and cultured muscle. Fresh normal fibres possessed extrajunctional ACh sensitivity covering several hundred micrometres around the end-plate and at the muscle-tendon junction. Myasthenia gravis affected fibres had reduced extrajunctional sensitivity at the end-plate and no detectable ACh sensitivity near the tendon.4. Less than one third of normal muscle bundles showed an increased area of ACh sensitivity after several days in organ culture. Under the same conditions myasthenic muscle bundles did not show an increase in extrajunctional ACh sensitivity,5. M.e.p.p.s were present for 2-4 days in normal fibres cultured at 36 degrees C. In normal and myasthenic muscles cultured at 23 degrees C m.e.p.p.s disappeared after 6-8 days and re-appeared in some fibres (50%) after approximately two weeks in organ culture. These m.e.p.p.s were abolished by curare and increased in frequency by hypotonic solution suggesting they are due to the release of ACh-packets from Schwann cells.6. Electron microscopic examination of cultured human muscle indicates that the disappearance of m.e.p.p.s corresponds with degeneration of nerve terminals.7. In muscle bundles shown to possess m.e.p.p.s after 13-14 days, the synaptic gutter, which had been vacated by the nerve terminal, was usually occupied by a Schwann cell or projections of Schwann cell cytoplasm. This indicates that the Schwann cell at denervated human end-plates may be capable of releasing packets of ACh.8. It is concluded that the organ culture system described here is suitable for studying normal and diseased human muscle fibres. Using this system we find that the denervation changes which follow nerve transection appear to be similar in most respects at normal and myasthenic end-plates.

Action Potentials↗
PubMed1982

Properties of junctional and extrajunctional acetylcholine-receptor channels in organ cultured human muscle fibres.

1. Current noise, obtained during steady ionophoretic application of acetylcholine (ACh) to voltage-clamped human fibres has been analysed to derive properties of end-plate channels and also extrajunctional ACh-activated channels which are present at the muscle-tendon junction of normal fibres. In addition, ACh-receptor channels present at the end-plate and tendon region in organ cultured muscles have been compared with those in fresh muscles.2. Extrajunctional channels in the tendon region of fresh fibres have a longer mean life-time, tau, and a smaller single channel conductance, gamma, than the junctional channels. tau was 1.71 +/-0.11 msec and gamma was 25.05 +/- 1.18 pS for junctional channels; tau was 3.16 +/- 0.33 msec and gamma was 12.76 +/- 1.29 pS for extrajunctional channels.3. Properties of channels in the end-plate and tendon region were unchanged during short-term (< 7 days) organ culture at 23 or 36 degrees C. The voltage sensitivity of the mean channel life-time was similar at junctional and extrajunctional sites.4. In muscles organ cultured for 7 days at 36 degrees C, double component noise spectra were obtained at some end-plates. The fast and slow time constants underlying the noise appeared to correspond to simultaneous activation of junctional and extrajunctional channels.5. After organ culture for 3-4 weeks at 23 degrees C the mean life-time of the end-plate channels was prolonged while their single channel conductance was unchanged, tau = 3.58 +/- 0.16 msec; gamma = 22.11 +/- 0.83 pS (V(m) = -80 mV, T = 21 degrees C).6. As end-plate channel properties were unchanged in short-term cultures it was possible to assess post-junctional sensitivity by comparing miniature end-plate current (m.e.p.c.) amplitudes in both normal and myasthenia gravis affected muscles. No evidence was found for a change in post-synaptic sensitivity during organ culture at 23 degrees C of normal or myasthenia gravis muscle fibres, which seems to rule out reversible block of receptors by anti-receptor antibody as playing an important role in myasthenia gravis.

Acetylcholine↗
PubMed1981

Induction of action potentials in frog slow muscle fibres paralysed by alpha -bungarotoxin.

Slow muscle fibres in the frog are normally incapable of generating action potentials. However, several days after an intramuscular injection of alpha - bungarotoxin, they acquire the ability to generate action potentials. It appears that alpha -bungarotoxin induces the action potential mechanism in slow fibres because it blocks acetylcholine receptors, and thus interferes with the action of non-quantal acetylcholine leaking from nerve terminals, or because the toxin has some other, as yet undefined, action on nerve or muscle.

Action Potentials↗
PubMed1981

Properties of postsynaptic channels induced by acetylcholine in different frog muscle fibres.

Skeletal muscles in the frog are composed of two distinct classes of muscle fibre: fast muscle fibres capable of propagating action potentials and twitches, and slow muscle fibres normally unable to generate action potentials or twitches. In addition, amphibian muscles contain a spectrum of 'intermediate' fibres whose structural and functional properties lie between those of fast and slow fibres. Much is now known about the characteristics of the channels opened by the transmitter acetylcholine (ACh) acting on the membrane of fast fibres, but the molecular action of ACh on the other fibre types is only poorly understood. We report here the existence of a muscle in the mandibular arch of the frog in which most, if not all, the fibres are multiply innervated and are capable of eliciting action potentials. We also report that the channels induced by the transmitter on the synaptic membrane of fast, slow and submaxillaris muscle fibres differ in their lifetimes and conductances.

Acetylcholine↗
PubMed1980

Visualization of satellite cells in living muscle fibres of the frog.

Satellite cells were visualized in living muscle fibres of the frog. Single fibres or bundles consisting of a few fibres were isolated after treatment with collagenase, and viewed under the light microscope. Subsequent electron microscopy of identified cells confirmed that they were satellite muscle cells. Under the light microscope, satellite cells appear as fusiform cells, tapering into long fine processes usually orientated parallel to the muscle fibre axis. Horseradish peroxidase injected into the muscle fibre was not transferred to the satellite cells.

Animals↗
PubMed1980

Induction of action potentials in cultured slow muscle fibres of the frog.

1. Slow muscle fibres of the frog were maintained in a simple organ culture system for up to 28 days at 18 degrees C. Slow fibres cultured for one week resembled innervated fibres in their lack of ability to generate an action potential. 2. By 10 days a few fibres had acquired the action potential mechanism and in muscles cultured for 28 days all slow fibres examined were capable of generating action potentials most of which reached or exceeded 0 mV membrane potential. 3. Slow muscle fibres which were denervated for two weeks in vivo retained their ability to generate overshooting action potentials after 4 weeks of culture. Thus, in the culture system described, slow muscle fibres are capable of developing action potentials and the action potential mechanism in these fibres remains for at least one month in culture.

Action Potentials↗
PubMed1980

On the release of transmitter at normal, myasthenia gravis and myasthenic syndrome affected human end-plates.

1. Transmitter release has been studied at normal, myasthenia gravis (m.g.) and myasthenic syndrome (m.s.) affected human end-plates. At normal and diseased end-plates evoked transmitter release is Poisson for a mean quantal content, m less than ten. 2. The relation between log m and log [Ca]o, at normal and m.g. end-plates is linear, with a slope of 3.3-3.4. The value of m at m.g. end-plates is about five times larger than normal, below Ca 0.7 mM (Mg, 2mM). This difference in m is reduced at higher Ca levels. 3. The slope of the relation between log m.e.p.p. frequency and log [K]o is similar at normal and m.g. end-plates. Over its linear portion the relationship has a slope of approximately 6. 4. Fluctuations in the latency of evoked transmitter release were compared at normal and m.g. nerve terminals. At normal end-plates the probability of release reaches a peak about 0.3-0.4 msec after unitary e.p.p.s of the shortest latency and returns to zero about 1.0 msec after the peak. At m.g. end-plates the distribution of latencies shows less uniformity. 5. At m.s. end-plates m is approximately 5 in normal Ringer solution (2 mM-Ca, 1 mM-Mg). The relation between log m and log [Ca]o is linear, with a slope of 1.0-1.5. The K dependence of m.e.p.p. frequency appears reduced at m.s. end-plates. 6. Assuming a co-operative mechanism for transmitter release at normal human motor nerve terminals, the dissociation constant for the Ca complex is about 1.6X10(-3) M and the dissociation constant for the Mg complex is about 1.0X10(-3) M. 7. It is concluded that the presynaptic changes, at m.g. end-plates, are not the primary cause of the defect in nerve muscle transmission. At m.s. end-plates the presynaptic changes are sufficient to account for failure in transmission. Possible mechanisms for the abnormalities in transmitter release are considered.

Action Potentials↗
PubMed1976

Reversible Inhibition of Potassium Contractures by optical isomers of verapamil and D 600 on slow muscle fibres of the frog.

Potassium-induced contractures were measured isometrically in slow fibres of gastrocnemius muscle from the frog Leptodactylus ocellatus. Optical isomers of verapamil and of D 600 decreased the tension of K-contractures with the following characteristics: 1. 90 min exposures of the muscles to the (-)isomers of the drugs were more effective in decreasing tension of 40 mM KCl-contractures when successive challenges to 40 mM KCl were made each 10-15 min than without challenges during the incubation time. 2. In contrast to the depressing effect of (-)isomers of verapamil and D 600, the decrease of K-contractures by 1 mM EGTA in "Ca-free" solutions was independent on the history of 40 mM KCl-contractures. 3. The threshold concentration of K to cause contractures was the lower the lower the Ca-concentration. This relationship was little affected by (-)verapamil at concentrations of the drug which depressed by 50% the tension of 40 mM KCl-contractures in 1.8 mM CaCl2. 4. Verapamil and its methoxy-derivative D 600 were equipotent in depressing 40 mM KCl-contractures. Their optical (-)isomers were 4 to 5 times more potent than their corresponding (+)isomers. 5. K-tension curves in the presence of 6.1 muM (-)verapamil in 1.8 mM CaCl2 were similar to curves in 0.18 mM CaCl2 without the drug. 6. K-tension curves in 10 mM CaCl2 were shifted by (-)verapamil in nearly parallel manner towards higher K-concentrations. 7. The stereoselective decrease of K-contractures by verapamil and D 600 may be due to blockade of inward Ca-flux and to retardation of the reavailability of Ca2+ for release during partial depolarizations with K.

Animals↗
PubMed1976

Potassium and calcium conductance in slow muscle fibres of the toad.

Slow muscle fibres in isotonic potassium sulphate saline could be easily repolarized to -90 mV. From this membrane potential a regenerative response could be elicited with short depolarizing pulses. 2. This response is blocked by TEA, suggesting that potassium is the main ion involved. 3. In the presence of TEA, a transient depolarization is recorded when the steady hyperpolarization is withdrawn. This anode break response is dependent upon the external calcium and is blocked by cobalt, suggesting that it is due to a calcium conductance. 4. The membrane conductance change was continuously recorded with short pulses at the end of the hyperpolarization. The membrane conductance decayed with at least two components with an average t1/2 of 1-2 and 6-8 sec. TEA blocked the slow component, and the fast one was dependent upon calcium and was blocked by cobalt.

Animals↗
PubMed1975

Development of supersensitivity in denervated slow muscle of the frog. Its dependence on the nerve stump length.

Sensitivity to carbachol has been studied in paired normal and denervated gastrocnemius slow muscle fibers of the frog. Dose response curves showed that after 25 days the ED50 was ten times less in denervated muscle than in the normal. The denervated muscle showed a three-fold increase in affinity constant to d-tubocurarine. In studying the development of supersensitivity of paired muscles denervated near or far from the neuromuscular junction it was found that muscles with a long axon stump started to increase sensitivity three days later than muscles with a short stump. We suggested that in slow muscle fibers, denervation supersensitivity is not only due to a spread in cholinergic receptor area but also to a change in the receptor properties. As the onset of the supersensitivity depends on the length of the nerve stump, it is also suggested that it is regulated by presynaptic factors which would be transported along the axon at a rate of a few centimeters per day.

Amputation Stumps↗
PubMed1974

Muscle contraction during hyperpolarizing currents in the crab.

Isolated muscle fibers from the motor legs of the crab Trichodactilus dilocarcinus were submitted to strong hyperpolarizing currents of varied intensities which produced tension during the current pulse. Threshold for tension was obtained with intensities of about 0.2 x 10(-5) A, changing E(m) to ca. -150 mV (starting from a resting potential ofca. -80 mV). At the closure of the anodic square pulse, a second phase of tension usually appeared superimposed upon the one obtained during hyperpolarization. The first phase of tension increased with the increase of Ca(++) concentration in the bath. Sr(++) produced the same type of mechanical output as Ca(++). When added to the normal Ca(++) concentration, Ba(++) and Mn(++) in low concentrations (up to 21.5 mM) also increased the tension of this phase, but at higher concentrations they blocked both phases while Mg(++) did not alter the tension. Of all the divalent cations employed, only Sr(++) is capable of developing tension as a substitute for Ca(++) in the external media. Procaine administered in a dosage (5 x 10(-3) W/V)which would suppress the contracture due to caffeine (10 mM), did not modify the tension developed during the hyperpolarization. The preceding data indicate that the Ca(++) required for tension during hyperpolarization comes from sites which would differ from those usually postulated for tension due to depolarization in the muscle fibers of other crustaceans (American crayfish). Furthermore, the external source of Ca(++) appears to be one mainly implicated in the induction of tension due to inward current pulses.

Animals↗