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A Lev-Tov

Publications and source records attributed to A Lev-Tov.

34 records · Page 2Linked to original sources
PubMed1988

The motor-unit population of the cat tenuissimus muscle.

1. We studied the organization of motor units in the tenuissimus (TEN) muscle of pentobarbital-anesthetized cats. The cat TEN is a long, delicate straplike muscle that spans hip and knee, which has a very flat length-tension curve through 22 mm of length change. 2. The TEN motor nucleus, labeled by retrograde transport of several forms of horseradish peroxidase, was composed of 8-31 cells in different cats, of which about half were, on average, in the size range of alpha-motoneurons. TEN motoneurons were scattered through the ventrolateral portion of lamina IX, over a rostrocaudal distance of up to 6.5 mm, making it relatively easy to isolate individual TEN motor axons for single motor-unit stimulation. 3. Individual TEN muscle units were classified into four groups [fast-twitch, fatigable (FF), intermediate, fatigue-resistant (Fint), fast-twitch, fatigue-resistant (FR), and slow-twitch, fatigue resistant (S)] on the basis of "sag" and fatigue index mechanical properties, as in other cat hindlimb muscles. There was a relatively large proportion of Fint units (28%) in the TEN sample, and the range of tetanic tension (approximately 19-fold) was much smaller than found in other cat hindlimb muscles. 4. A majority of TEN muscle fibers could be classified into the three major histochemical types (IIB, IIA, and I) found in other cat muscles, but a substantial minority remained "unclassified." A single type Fint muscle unit was successfully depleted of glycogen for histochemical study. It exhibited a typical type IIB histochemical profile. 5. Despite its unusual morphology, the cat TEN contains the same types of motor units found in larger, more "typical" limb muscles.

Acetylcholinesterase↗
PubMed1987

Junctional transmission in fast- and slow-twitch mammalian motor units.

The phenomena of facilitation and tetanic potentiation of end-plate potentials (EPPs) were investigated in the predominantly fast-twitch extensor digitorum longus (EDL) and the predominantly slow-twitch soleus (Sol) muscles of the rat, using extra- and intracellular recording methods. When the quantal content of the EPPs was reduced to average values of 2-3, facilitation and potentiation could be studied in both muscles without the masking effects of neuromuscular depression. Under these conditions, the facilitation and potentiation at the neuromuscular junctions of EDL were different from those at the junctions of Sol. The potentiation during sustained activation was higher in EDL than in Sol at stimulation frequencies varying between 10 and 100 Hz. The same tendency was found for the facilitation measured by paired stimuli; the facilitation in EDL was generally higher than in Sol with interpulse intervals between 300 and 10 ms. The dependence of facilitation and potentiation on the stimulation frequency was also different in EDL and Sol. As the interpulse interval decreased from 200 to 25 ms, the facilitation in Sol increased more steeply than in EDL, whereas with further decrease from 25 to 10 ms, the facilitation in Sol did not increase at all, whereas the facilitation in EDL exhibited a substantial increase. The same general pattern was observed for potentiation: the potentiation in Sol increased more steeply than in EDL between 10 and 40 Hz (100- to 25-ms intervals) and more moderately than in EDL between 40 and 100 Hz (25- to 10-ms intervals). Another paradigm, repetitive short trains, induced a progressive increase in potentiation at the neuromuscular junctions of both muscles. The cumulative effect of potentiation was more prominent in EDL than in Sol. The differences in potentiation between EDL and Sol were also evident from intracellular recordings. These recordings also revealed that the amplitude of miniature EPPs remained unaltered in both muscles before and during the stimulus trains. Comparisons of the EPPs elicited before and at the end of tetanic trains revealed that the onset time of the EPPs was delayed in Sol but not in EDL during the train. This latency shift was also observed in the focally recorded nerve terminal potentials and end-plate currents in Sol, but not in EDL. The differences in facilitation and potentiation between EDL and Sol may be due to heterogeneities of the transmitter release machinery of their nerve terminals or differences in the capability of their presynaptic nerves to conduct action potentials at high frequencies.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

The organization and activity patterns of the anterior and posterior heads of the guinea pig digastric muscle.

The structure and activity patterns of the anterior and posterior heads of the guinea pig digastric muscle (DG) were studied in ketamine-anesthetized guinea pigs. Collagen staining of longitudinal and transverse sections of the muscle revealed that the guinea pig DG is comprised of a unicompartmental anterior head (ADG) and a multicompartmental posterior head (PDG). The two heads are separated by a thin tendinous inscription that, unlike the intermediate tendon of the DG in humans, is not attached to the hyoid bone. The motor nuclei of the guinea pig DG were reconstructed using retrograde labeling with horseradish peroxidase. The motoneurons of the ADG were clustered in a longitudinal column within the trigeminal motor nucleus. The motoneurons of the PDG were segregated into two clusters within the facial motor nucleus. The cross-sectional areas of the ADG and PDG motoneuron somata exhibited unimodal frequency distributions and the average soma area was larger for ADG than PDG motoneurons. Histochemical characterization of ADG and PDG revealed that the two muscle heads contained the three main histochemical types of muscle fibers identified in limb muscles. The frequency distribution of fiber types in ADG and PDG were not significantly different. Both muscle heads were predominantly fast with slow oxidative fibers accounting for only 1.1 and 0.3% of the fibers in narrow dorsal regions of ADG and PDG, respectively, and 13.6 and 12.9% in the more ventral regions of ADG and PDG, respectively. Simultaneous recordings of EMGs from the ADG and PDG were carried out during spontaneously occurring rhythmical jaw movements. These recordings revealed a high degree of synchrony between the activities of the two heads, although differences were observed in the onset and duration of the EMG bursts. Activity in the PDG preceded activity in the ADG in most of the rhythmical cycles and persisted longer. The differences in latencies of time-locked EMGs evoked in the ADG and PDG by four-pulse cortical stimulation were much smaller than those observed between the activity bursts of the two heads during rhythmical jaw movements. It is suggested that the early activity in the PDG is accounted for by shorter central conduction times in the pathways onto it and/or by higher recruitability of its motor units. The early activity in PDG may serve to optimize the location of ADG on its length-tension curve prior to and during the active state.

Animals↗
PubMed1986

The modulation of transmitter release in motor nerve endings varies with the type of muscle fiber innervated.

Electrophysiological studies of synaptic transmission in mammalian muscles revealed substantial differences between neuromuscular synapses associated with fast versus slow-twitch motor units. Synapses of fast units exhibited much higher tetanic and post-tetanic potentiation of neurotransmitter release than those of slow units. On the other hand, the tetanic potentiation of slow units increased faster as a function of the frequency of activation than that of fast units. These differences suggest a possible specialization of neuromuscular synapses with the type of motor units they are associated with.

Acetylcholine↗
PubMed1984

Peripheral and central control of flexor digitorum longus and flexor hallucis longus motoneurons: the synaptic basis of functional diversity.

The two long toe flexor muscles in the cat, flexor digitorum longus (FDL) and flexor hallucis longus (FHL), have essentially identical mechanical actions, yet are used very differently during locomotion (O'Donovan et al. 1982). We attempted to identify the origin of the synaptic drive responsible for this functional differentiation. The organization of peripheral and central synaptic drive to FDL and FHL motoneurons was examined using two basic paradigms. (1) In animals anesthetized with chloralose or after ischemic destruction of the brain, peripheral reflex circuits were studied by recording intracellular responses from alpha-motoneurons produced by electrical stimulation of muscular and cutaneous nerves. (2) "Fictive locomotion", the centrally generated rhythmic synaptic drive produced in paralyzed, decerebrate animals by stimulation of the mesencephalic locomotor region or intravenous injection of L-DOPA and Nialamide, was monitored by recording electroneurograms from the central end of cut motor nerves. Despite their functional dissimilarity, FDL and FHL motoneurons received monosynaptic EPSPs from both FDL and FHL la afferents. Ipsilateral cutaneous afferents in the sural nerve and from the central plantar pad produced multiphasic PSPs which were not different in FDL and FHL cells. However afferents from the saphenous and superficial peroneal nerves did exert differential effects: the first component of the multiphasic PSP in most FDL cells was an EPSP, which was not present in most FHL cells. The central latency of this early EPSP in FDL motoneurons (0.8-1.5 ms) strongly suggests a disynaptic linkage. Cutaneous afferents from the ipsilateral forelimb produced IPSPs in most FHL cells but in only one of 18 FDL cells. Since some peripheral reflex circuits exerted differential effects on FDL and FHL cells, but others did not, the intracellular data did not demonstrate that the functional differences between FDL and FHL could be explained by differences in reflex organization. During fictive locomotion elicited by electrical or pharmacological stimulation, FHL motoneurons were coactive with ankle extensors during the extension phase of the fictive step cycle. In contrast, FDL motoneurons were most consistently activated in a brief burst at the onset of the flexion phase, showing much weaker and more variable coactivity with ankle extensors. These patients were essentially identical to those reported for FDL and FHL motor pools during treadmill locomotion by O'Donovan et al. (1982). We conclude that the central pattern generator (CPG) for locomotion produces distinct and highly differentiated sets of instructions for FDL and FHL motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1983

Posttetanic potentiation of group Ia EPSPs: possible mechanisms for differential distribution among medial gastrocnemius motoneurons.

We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group Ia monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) alpha-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Lüscher and colleagues (43, 44) of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (Pmax) and 1) the mean amplitude of the pretetanic control EPSP in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as "differential distribution of PTP" within the MG motor pool, were less strong in the present work than reported by Lüscher et al. (43, 44). We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of Pmax subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as "specific" synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the nonlinear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.

Animals↗
PubMed1983

Factors that control amplitude of EPSPs in dendritic neurons.

We have used a computer-based mathematical model of alpha-motoneurons and of group Ia synaptic input to them, based on anatomical and electrophysiological data from the cat spinal cord, in order to examine the effects of variations in neuron size and input resistance and of conductance magnitude and duration on the generation of excitatory postsynaptic potentials (EPSPs). The first set of calculations were designed to test the possible role of nonlinear EPSP summation in producing a differential distribution of posttetanic potentiation of group Ia EPSPs, described in the preceding paper (25; see also Refs. 26, 27). The results suggest that the negative correlations observed between the degree of posttetanic potentiation of Ia EPSPs and initial (pretetanic) EPSP amplitude as well as with the input resistance of the postsynaptic motoneurons can be explained in part by the inherent non-linearity between conductance change and the resultant potential change at chemical synapses. In a second set of calculations, we used the same model system to evaluate the effects produced by variations in neuronal membrane area, input resistance, and specific membrane resistivity, as well as of the density of excitatory synaptic input on the peak amplitude of EPSPs. With parameters constrained to match the properties of alpha-motoneurons and group Ia synaptic input, EPSP amplitudes were most sensitive to changes in synaptic density and were much less sensitive to alterations in neuron input resistance and specific membrane resistivity when synaptic density was constant.

Animals↗
PubMed1982

A HRP study of the relation between cell size and motor unit type in cat ankle extensor motoneurons.

The dimensions of the somata and stem dendrites of 57 alpha- and three gamma-motoneurons, identified as to motor unit type and labeled by intracellular injection of horseradish peroxidase, were measured in the triceps surae and plantaris motor pools. The somata of type S motoneurons tended to be smaller (mean diameter 47.9 micrometers) than those of FF and FR units (52.5 and 53.1 micrometer, respectively) but these mean values were not significantly different and the data distributions showed considerable overlap between the unit types. The mean numbers and diameters of stem dendrites exhibited somewhat larger differences related to motor unit type and some of these were statistically significant. The total membrane area (AN) of each cell was estimated from measurements of the soma and stem dendrites, by using recent data and Ulfhake and Kellerth ('81) to calculate the membrane area of a dendritic tree from stem dendrite diameter. Mean AN varied with motor unit type in the sequence FF greater than FR greater than S (average values: 369 X 100(3) micrometers 2, 323 X 100(3) micrometers 2, and 250 X 100(3) micrometers 2, respectively). There was covariation between AN and the conduction velocity of the motor axon as well as with the force output from the muscle unit. Comparison of AN and motoneuron input resistance (RN) in 19 alpha-motoneurons suggested that the specific resistivity of the cell membrane in type S motoneurons was systematically higher than that characteristic of type FF or FR motoneurons.

Animals↗
PubMed1982

Regulatory role of intracellular sodium ions in neurotransmitter secretion.

Calcium ions are the main inducer of quantal transmitter release of the frog neuromuscular junction; but even in their virtual absence from the extracellular medium, nerve stimulation causes a prolonged augmentation of transmitter release. These facts led to the hypothesis that an accumulation of intracellular sodium can serve as a slow secondary regulator of neurosecretion. Three lines of evidence presented in this article substantiate this hypothesis: firstly, veratridine, which is known to increase sodium fluxes through the voltage-dependent sodium channels, increases transmitter release after nerve stimulation. Secondly, monensin, which was shown to induce sodium transport through nerve membranes, increases evoked transmitter release, tetanic potentiation and posttetanic potentiation. Thirdly, sodium-filled phosphatidylcholine liposomes increase transmitter release. These effects of sodium are probably not due to a direct effect on the transmitter release mechanism, but are caused by sodium-induced calcium translocation from intracellular stores.

Animals↗
PubMed1980

A study of tetanic and post-tetanic potentiation of miniature end-plate potentials at the frog neuromuscular junction.

1. The involvement of calcium sodium, potassium and magnesium in tetanic and post-tetanic potentiation of miniature end-plate potential frequency was examined at the frog neuromuscular junction using conventional electrophysiological techniques. 2. Tetanic potentiation is larger in calcium containing solutions, than in solutions which generate reversed electrochemical gradient for calcium during nerve activity. 3. Tetanic potentiation increases with stimulation frequency and duration, under both inward and reversed electrochemical gradient for calcium conditions. This indicates that factors, other than calcium entry, participate in tetanic potentiation. 4. Addition of the potassium conductance blocking agent, 3-aminopyridine (5 mM), increases tetanic potentiation in calcium containing media, while depressing it under reversed calcium gradient. 5. Electronic depolarization of the nerve terminal in tetrodotoxin-containing Ringer solution, produces tetanic potentiation under inward gradient, but fails to do so under reversed gradient. This indicates that the entry of sodium ions participates in the generation of tetanic potentiation. 6. Addition of magnesium ions suppresses tetanic potentiation in calcium containing solution, but increases tetanic potentiation under reversed gradient. 7. The results are explained by the hypothesis that calcium entry and intracellular calcium translocation participate in the generation of tetanic potentiation. 8. Both the fast and the slow components (augmentation and potentiation respectively) of post-tetanic potentiation increase in duration, with increase in the tetanic stimulation rate. 9. The decay of post-tetanic potentiation increases: when [Ca]o is elevated by ionophoretic application during the decay phase only, when ouabain is present in the medium or when [Mg]o is elevated. These finding suggest that calcium, sodium and possibly magnesium take part in post-tetanic potentiation.

Animals↗
PubMed1980

Regulation of acetylcholine liberation from presynaptic nerve terminals.

Acetylcholine is liberated from motor nerve terminals either as a molecular leakage or as quantal packages; the latter form of release is responsible for signaling across the neuromuscular synapse. Three main factors determine the number of quanta liberated by the nerve impulse: the degree of presynaptic depolarisation, the frequency of activation of the nerve terminal, and calcium ion concentration in the extracellular medium. These factors seem to act yb changing the free calcium ion concentration [Ca]in in the presynaptic nerve terminal. Thus, processes that change [Ca]in will determine efficiency of synaptic transmission. These processes include fluxes of calcium ions across the presynaptic membrane and reversible translocation by intracellular organelles such as mitochondria, vesicles and soluble molecules. The level of intracellular [Ca] can be changed by ion-containing liposomes. One of the main physiological determinants of the level of transmitter release is potentiation, where the increase in transmitter release is caused by transmembranal processes and intracellular translocation.

Acetylcholine↗
PubMed1980

Primary and secondary regulation of quantal transmitter release: calcium and sodium.

Calcium is the prime regulator of quantal acetylcholine liberation at the neuromuscular junction; its entry through the presynaptic membrane and the level of free [Ca]in most probably determine the number of transmitter quanta liberated by the nerve impulse. The level of free [Ca[in, in turn, is controlled by a number of subcellular elements: mitochondria, endoplasmic reticulum, vesicles, macromolecules and the surface membrane. The action potential induced calcium entry is not the only factor responsible for coupling nerve terminal depolarization with increased transmitter release; increased transmitter release occurs also in the virtual absence of calcium ions in the extracellular medium, when a reversed electrochemical gradient for calcium probably exists during action potential activity. Several lines of evidence suggest that the entry of sodium ions is responsible for this augmented transmitter release: the tetanic potentiation observed under reversed calcium gradient is blocked by tetrodotoxin; tetanic and post-tetanic potentiation are augmented and prolonged by ouabain; the amplitude of the extracellular nerve action potential is reduced with high-frequency stimulation, in parallel with increased spontaneous quantal release. In addition, sodium-filled egg-lecithin liposomes augment quantal liberation. The augmentory effect of sodium on transmitter release is probably due to an intracellular calcium translocation, since no preferred timing after the action potential is observed. Thus, the level of [Na]in in the presynaptic nerve terminal can control indirectly the efficiency of synaptic transmission.

Acetylcholine↗
PubMed1978

Intracellular and extracellular calcium ions in transmitter release at the neuromuscular synapse.

The theme of this presentation has been to show that the control of transmitter release at the neuromuscular synapse is achieved by extracellular and intracellular calcium. For the fast information transfer represented by the end-plate potential, the electrochemical gradient for calcium across the presynaptic membrane and the associated calcium conductance seem to play the primary role. For slower processes such as tetanic and posttetanic potentiation, the combined effect of both sources for calcium determine the amount of transmitter liberated.

Acetylcholine↗