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At least 1,369 records · Page 76Linked to original sources
PubMed2002

Sphingosine 1-phosphate enhances spontaneous transmitter release at the frog neuromuscular junction.

Intracellular recordings were made from isolated frog sciatic-sartorius nerve-muscle preparations, and the effects of sphingosine 1-phosphate (S1-P) on miniature endplate potentials (MEPPs) were studied. Extracellular application of S1-P (1 and 30 micro M) had no significant effects on the frequency and amplitude of MEPPs. Delivery into nerve terminals by liposomes containing 10(-5), 10(-4) or 10(-3) M S1-P was associated with a concentration-dependent increase in MEPP frequency of 37, 63 and 86%. The per cent of median MEPP amplitude was not significantly changed, but there was an increase in the number of 'giant' MEPPs. Pre-exposure of the preparations to S1-P 10(-5) but not 10(-8) M entrapped in liposomes for 15 min blocked the effects of subsequent superfusion of S1-P (10(-4) M)-filled liposomes on MEPP frequency. Thus, intracellular S1-P receptors seem to undergo 'desensitization' to higher concentrations of S1-P. The result provides the first evidence that S1-P acting intracellularly but not extracellularly enhances spontaneous transmitter release at the frog neuromuscular junction.

Animals↗
PubMed1956

Changes in the duration of the electric response of single nerve fibers following repetitive stimulation.

Single nerve fibers were isolated from the nerve innervating the sartorius or semitendinosus muscle of the toad (Bufo marinus). Single nerve fiber responses were recorded with three arrangements of the "bridge insulator" method. During stimulation at 50 to 150 pulses per second for 20 to 140 minutes the spike duration was progressively increased. After tetanization the spike duration usually continued to increase at a more rapid rate. Within 5 to 60 minutes further prolongation stopped and within 1 to 10 hours the spike duration was normal. The duration of the response of tetanized fibers was from 2.5 to more than 10 times the spike duration of untetanized fibers. Prolongation was observed in nerve fibers isolated from nerves tetanized in vivo.

Electric Stimulation↗
PubMed1966

Topochemical factors in potentiation of contraction by heavy metal cations.

In addition to the previously studied Zn(2+), low concentrations (about 0.5 mM) of Be(2+), Ba(2+), Cd(2+), Ni(2+), Cu(2+), Pt(4+) and, outstandingly, 0.5 microM of UO(2) (2+), potentiate the twitch of frog sartorius and toe muscles by prolonging the active state of contraction. The degree of potentiation is a roughly S-shaped function of p(metal(2+)), suggesting that each metal binds to a ligand of the muscle fiber, representative apparent affinity constants being: UO(2) (2+), 5 x 10(6); Zn(2+), 2.8 x 10(5); and Cd(2+), 2 x 10(4). UO(2) (2+) potentiation effects are rapidly reversed by PO(4), and Zn(2+) and Cd(2+) effects by EDTA, PO(4), and cysteine. The rapidity of these reversals by the nonpenetrating EDTA and PO(4), and the fact that heavy metal ions evidently potentiate by prolonging the action potential, indicate that the metal potentiators exert their primary action at readily accessible (i.e. plasma and T tubular) membrane sites. The relatively slow kinetics of development of potentiation, and the even slower reversal of it in pure Ringer's solution, indicate that the metal ions are bound to connective tissue, as well as to muscle fibers. The binding effects at the readily accessible membrane sites evidently impairs delayed rectification and thus modifies the action potential and excitation-contraction coupling so as to cause potentiation. SH is excluded, and PO(4) and imidazole are possibilities, as the membrane ligand binding the potentiating metal ions.

Animals↗
PubMed1973

Some effects of dimethyl sulphoxide (DMSO) on the frog neuromuscular junction.

1. Dimethyl sulphoxide (DMSO) partially reversed neuromuscular blockade brought about by the action of (+)-tubocurarine or Mg(2+) on the frog sartorius nerve-muscle preparation.2. The amplitude and duration of the endplate potential (e.p.p.) were increased by DMSO at concentrations of 70 mM or greater.3. Miniature endplate potentials were raised in frequency, prolonged in duration and increased in amplitude by DMSO at concentrations of 141 mM or greater, but the increase in amplitude was generally less than in the case of the e.p.p.4. The resting muscle membrane potential was significantly depolarized by DMSO at 70 mM or greater concentrations, both at the endplate and remote from an endplate.5. The reversal of neurmuscular blockade by DMSO can be explained in terms of its previously reported ability to inhibit cholinesterase activity, together with the depolarizing action on muscle.

Animals↗
PubMed1979

A comparison of the facilitatory actions of 4-aminopyridine methiodide and 4-aminopyridine on neuromuscular transmission.

1 4-Aminopyridine methiodide (4-APMI), a quaternary analogue of aminopyridine (4-AP), was tested for neuromuscular facilitatory actions on the chick biventer cervicis and frog sartorius nerve-muscle preparations. 2 In the chick, 4-APMI (10(-4) to 10(-2) M) augmented indirectly elicited twitches and reversed tubocurarine-induced neuromuscular block. Reversal of tubocurarine block was observed after treatment of the muscle with an anticholinesterase. 4-APMI did not itself produce contracture but augmented responses to added acetylcholine. 3 4-APMI (10(-4) M) prolonged the time courses of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) in the frog. 4 4-APMI (10(-4) M) increased e.p.p. quantal content. 4-AP was about 100 times more active than 4-APMI in increasing quantal content. Both compounds prolonged muscle action potentials at similar concentrations. 5 4-APMI (10(-3) to 3 X 10(-3) M) possessed anticholinesterase activity in homogenates of chick biventer cervicis muscle. 6 It is concluded that 4-APMI increases evoked acetylcholine release and also possesses a weak anticholinesterase action. The greater action of 4-AP on quantal content is probably due to an intracellular action, possibly involving the release of calcium ions.

Action Potentials↗
PubMed1972

The effect of voltage on the time course of end-plate currents.

1. End-plate currents have been studied in glycerol-treated frog sartorius nerve-muscle preparations with the voltage clamp technique.2. End-plate currents follow a simple exponential time course over most of their declining phase.3. The rate constant alpha that characterizes this exponential decay depends upon membrane potential V according to the relationship alpha (V) = Be(AV), with A = 0.00795 +/- 0.00043 (S.E.) mV(-1) and B = 1.67 +/- 0.04 (S.E.) msec(-1).4. Voltage sensitivity decreases (that is, A in the above equation becomes smaller) as the recording and current-passing electrodes are moved away from the end-plate region.5. The voltage sensitivity of alpha is decreased by decreasing the gain of the voltage clamp amplifier.6. Changing the end-plate current amplitude by curare treatment, by increased calcium ion concentration, and by facilitation and depression has essentially no effect on end-plate current time course.7. When membrane potential is changed step-wise during the decaying phase of the end-plate conductance change, currents begin to decline with a rate constant alpha appropriate to the new membrane potential in less than 0.2 msec.8. Treatment with prostigmine methylsulphate in concentrations up to 50 mug/ml. slows end-plate current decay but has little effect on voltage sensitivity. That is, B in the above equation is decreased by prostigmine treatment, but A is relatively unaffected.

Action Potentials↗
PubMed1972

A quantitative description of end-plate currents.

1. End-plate currents have been studied in glycerol-treated frog sartorius nerve-muscle preparations with the voltage clamp technique.2. The effects of temperature on the decay rate of end-plate currents were investigated over a temperature range from 10 to 30.5 degrees C. The Q(10) for the decay constant of end-plate currents depends somewhat on membrane potential; at - 100 mV the decay constant has a Q(10) of 2.7.3. Peak end-plate current depends non-linearly on membrane potential with a decreasing slope conductance associated with hyperpolarization.4. The ;instantaneous' voltage-current relationship for end-plate channels was determined by causing step changes in membrane potential during end-plate current flow. This relationship appears to be linear.5. The interaction of acetylcholine with its receptor is viewed as being analogous to the first step in enzymic catalysis. On this view, acetylcholine binds to its receptor and induces a conformational change which is responsible for opening end-plate channels. By analogy to the first steps in the catalytic sequence of enzymes, the binding step is very rapid, almost diffusion-limited, and the conformational change is rate-limiting.6. Equations describing this process have been derived. Expressions for the rate constants have also been derived by considering changing dipole moments of the transmitter-receptor complex associated with the conformational change. As the transmitter-receptor complex is in the membrane field, different conformational states have different energies, and the rate of conformational change thus depends on membrane potential. The equations thus derived are shown to account adequately for the time course of end-plate conductance change.

Acetylcholine↗
PubMed1975

Factors affecting the time course of decay of end-plate currents: a possible cooperative action of acetylcholine on receptors at the frog neuromuscular junction.

1. End-plate currents have been studied in gylcerol-treated frog sartorius nerve-muscle preparations with the voltage-clamp technique. 2. Adding the anticholinesterase prostigmine (3 muM) to the solution bathing the muscle caused a 2-7 (mean 3-3) times increase in the time constant of decay of end-plate currents. The anticholinesterase edrophonium (15 muM) also prolonged the time course of end-plate currents. 3. Pre-treatment of the preparation with collagenase, which leads to the removal of acetylcholinesterase in the synaptic cleft, prolongs the time course of end-plate currents. 4. Curare (1-2 muM), cobratoxin (0-13 muM), or alpha-bungarotoxin (0-13-0-26 muM) decreased the time constant of decay of end-plate currents in the presence of prostigmine. 5. These observations are consistant with the suggestion that repeated binding of acetylcholine (ACh) molecules to receptors as the ACh escapes from the synaptic cleft can contribute to the prolongation of end-plate currents which occurrs when acetylcholinesterase activity is eliminated. 6. Increasing the amount of transmitter released from the presynaptic nerve terminal leads to a prolongation of end-plate currents in the presence of prostigmine. 7. In the presence of prostigmine, the second of two end-plate currents (interval 2-10 msec) decays more slowly than the first. 8. ACh (1-40 muM) or carbachol (40 muM) applied in the solution bathing the muscle prolongs end-plate currents in the presence of prostigmine. 9. It is suggested on the basis of the observations described in paragraphs 6 to 8 that the time constant of decay of end-plate currents in the presence of prostigmine increases with increasing concentrations of ACh in the synaptic cleft. In the absence of prostigmine, increasing the concentration of ACh in the synaptic cleft did not change the time constant for decay of end-plate currents. 10. We interpret these results to suggest that ACh can have a cooperative action on receptors such that the association of ACh with one receptor (defined as binding a single ACh molecule) favours the binding or retention of ACh at other receptors. This implies that receptors can interact.

Acetylcholine↗
PubMed1976

A voltage-clamp study of the effect of two lidocaine derivatives on the time course of end-plate currents.

1. Voltage-clamped end-plate currents (e.p.c.s) have been studied in the glycerol-treated Rana pipiens sartorius nerve-muscle preparations in normal Ringer solution and in the presence of QX-222 and QX-314. 2. Both QX-222 and QX-314, the trimethyl and triethyl analogues, respectively, of lidocaine, greatly modify end-plate current kinetics. The altered e.p.c.s still show a true reversal potential, which is essentially the same as the reversal potential before drug treatment. The time course of the altered end-plate currents varies with both membrane potential and drug concentration. 3. In the presence of 0-1-1-0 mM QX-222, end-plate currents decay as the sum of three exponentials: I(t) =I1(0)e-k1t+I2(0)e-k2t+I3(0)e-k3t, where the subscipts 1, 2 and 3 refer to the rapidly, intermediately, and slowly decaying components, respectively. Both the amplitudes, Ij(0), and the decay rates, kj, depend upon membrane potential. 4. Hyperpolarization increases the relative size of the first and third components, i.e. I1(0) and I3(0) increase relative to I2(0). Depolarization increases the relative size of the second component. 5. Hyperpolarization causes a decrease in the decay rates k2 and k3 and causes a slight increase in the decay rate k1. Dependence of the three decay rates on membrane potential is well described by: kj=bjeajv. 6. The Q10 of each of the kj is about 3. 7. Raising QX-222 concentration, at any given membrane potential, augments I1(0) and I3(0) at the expense of I2(0). Raising concentration increases k1 and decreases k3; their voltage-dependence is little affected. 8. At all QX-222 concentrations tested the decay rate k2 is nearly the same as the decay rate of a normal e.p.c. recorded at an equivalent holding potential from the same fibre before drug exposure. 9. End-plate currents in the presence of 0-1 mM-QX-314 show a "major" or rapidly decaying phase and a very small, slowly decaying phase or "tail", but no intermediate component. Only the major component is discernible for end-plate currents in 0-5 mM-QX-314. 10. Voltage- and concentration-dependence of the decay rate of the major component in QX-314 is similar to k1 and QX-222. Voltage-dependence of the tails decay rate appears to be similar to k3. It is hypothesized that the second component in QX-222 represents currents of unaltered or normal conductance kinetics, and that the first and third components in QX-222, as well as the major component and tail in QX-314, represent current of "QX-altered conductance kinetics".

Animals↗
PubMed2003

Extra- and intracellular sphingosylphosphorylcholine promote spontaneous transmitter release from frog motor nerve endings.

Similar to phosphatidylinositol bisphosphate, sphingomyelin breakdown generates several lipids, including sphingosylphosphorylcholine (SPC), that are putative signaling molecules. The present study was undertaken to evaluate the involvement of SPC in transmitter release process. Intracellular recordings were made from isolated frog sciatic-sartorius nerve-muscle preparations, and the effects of SPC on neurosecretion in the form of miniature endplate potentials (MEPPs) were assessed. Extracellular application of SPC mixture (D,L-SPC) at 1, 10, and 25 microM increased the MEPP frequency by 68, 96, and 127%, respectively. D-erythro-SPC (dissolved in dimethyl sulfoxide but not coupled to bovine serum albumin), but not L-threo-SPC, was active extracellular; the former (at 10 microM) increased the MEPP frequency by 143%. D-erythro-SPC treatment did not significantly change the median amplitude or frequency-distribution of MEPPs. Intracellular delivery via liposomes, in which 10, 100, or 1000 microM SPC mixture was entrapped in liposomal aqueous phase, induced a concentration-dependent increase in MEPP frequency of 45, 91, and 100%, respectively. D-erythro-SPC and L-threo-SPC at the concentration of 100 microM increased the MEPP frequency by 117 and 67%, respectively, or 91 and 61%, respectively, when coupled to bovine serum albumin. Pretreatment with thapsigargin significantly reduced but did not abolish the effects of extracellular D-erythro-SPC (10 microM) or liposomes containing 100 microM D-erythro-SPC. Liposomes filled with 100 microM D-myo-inositol 1,4,5-trisphosphate (IP3) enhanced the MEPP frequency to the same magnitude as 100 microM D-erythro-SPC entrapped in liposomes. However, administration of 100 microM D-erythro-SPC and IP3 entrapped in the same liposomes enhanced the MEPP frequency by 70%, which was less than that produced by these two compounds alone. The result provides the first electrophysiological evidence that SPC can modulate transmitter release by an extra- or intracellular action at the frog motor nerve ending.

Animals↗
PubMed1990

Focal fibrocartilaginous dysplasia associated with tibia vara.

Focal fibrocartilaginous dysplasia of the tibia at the insertion of the pes anserinus (the expanded tendinous insertion of the gracilis, sartorius, and semitendinous muscles) is a rare unilateral lesion with a characteristic deformity of the proximal tibial metadiaphysis. It is associated with unilateral tibia vara in toddlers. Three cases of this entity are described, and the radiologic features are presented. Recognition of this disease is important because the response to conservative therapy is excellent.

Child, Preschool↗
PubMed1990

Growth and metabolism in somatotropin-treated steers: III. Protein synthesis and tissue energy expenditures.

Rates of in vivo protein synthesis in intercostal, sartorius and semitendinosus muscle and in the heart, liver, kidneys, rumen and jejunum were determined in 20 growing Hereford steers treated for 112 d with daily subcutaneous injections of either saline (S) or recombinantly derived bovine somatotropin (rBST; 20.6 mg/d). In vitro rates of protein synthesis and energy expenditures associated with Na+, K+ transport also were determined in external intercostal muscle, liver, kidneys and jejunum. Neither in vivo nor in vitro tissue protein fractional synthetic rates (mg/[g protein.d]), using either the plasma (P) or intracellular fluid (ICF) phenylalanine specific radioactivity for the precursor pool, were affected by rBST treatments. Energy expended on Na+, K+ transport was greater (P less than .1) in the livers of rBST-treated steers, which would increase the maintenance energy expenditures of these steers. Protein accretion rates in the liver, kidneys, stomach, hide, and head, feet and tail of rBST-treated steers were greater (P less than .05) than in S steers. Tissue amino acid profiles were not affected by rBST treatments except in the rumen, where profiles suggested that less collagen was present in rumen wall tissue protein of rBST steers. Plasma phenylalanine entry rates also were not affected by rBST treatment; muscle protein synthesis accounted for a minimum of 20% of this entry rate.

Animals↗
PubMed1984

Electrophysiological and neurochemical investigations of the action of presynaptic neurotoxins.

Previous experiments have suggested that hemicholinium-3 might directly antagonize certain actions of beta-bungarotoxin at the neuromuscular junction. Data presented here show that, on the contrary, hemicholinium-3 neither inhibits the phospholipase activity of beta-bungarotoxin nor does it affect the characteristic pattern of transmitter release observed at end plates exposed to the toxin. Lanthanum ions were found to promote the release of acetylcholine from sartorius nerve-muscle preparations that had been paralyzed by botulinum toxin. However, the acceleration of transmitter release by lanthanum was not nearly as great as in control preparations as monitored either electrophysiologically or by chemical measurement of ACh.

Acetylcholine↗
PubMed1996

[Applied anatomy of the medial superior genicular artery and the retrograde island flap].

Through anatomical dissection of fifty freshly amputated adult lower extremities, the origin, length, diameter and extent of perfusion of the superior genicular artery and its relation with the anterior tibial recurrent artery were investigated. Results revealed that the medial superior genicular artery originated primarily from the femoral artery (95.5%). It descends between the sartorius and majormedial muscles and then separates into branches that nourish the upper one-third of the lower leg and the medial skin of the knee, and then, by anastomosis, joins the anterior tibia recurrent artery on the level of the medial malleolus of the tibia. The formation rate of the anastomotic arch is 100% with the average outer diameter of 1.3 +/- 0.39 mm (x +/- s). Based on these observations, we conclude that the medial area of the knee is the best donor site of an island flap, which can be used to repair the medial superior one-third of the lower leg and the region around the knee.

Adolescent↗
PubMed1996

Passive knee muscle moment arms measured in vivo with MRI.

OBJECTIVE: To determine moment arm lengths from seven knee muscles and the patellar tendon. The knee muscles were the biceps femoris, semitendinosus, semimembranosus, gracilis, sartorius, and the lateral and medial gastrocnemius muscles. DESIGN: The moment arms were calculated based on MRI measurements. BACKGROUND: Moment arm lengths of different muscles with respect to the joint centre of rotation (CR) or the centre of the contact point between joint surfaces are necessary basic data for biomechanical models predicting joint load. METHODS: Ten male and seven female subjects participated. Using a 1.5 Tesla magnetic resonance imaging system, 3-dimensional coordinates of relevant points were recorded from a 3-D volume reconstruction of the right knee at knee flexion angles of 0, 30 and 60 degrees. Muscular moment arms were calculated in both the sagittal and frontal planes. The recordings were all made during passive mode, which means that no muscular contraction was performed. RESULTS: All muscles except the lateral gastrocnemius showed statistically significant differences (P<0.05) of moment arm lengths between gender in the frontal plane. All muscles except biceps femoris and sartorius showed significant differences (P<0.05) of moment arm lengths between gender in the sagittal plane. Most muscles also showed a linear or quadratic trend of changing moment arms with varying knee angle. CONCLUSIONS: Our results indicate that for most biomechanical analyses involving knee muscles, gender- and angle-specific moment arms should be used.

Journal Article↗
PubMed1991

Neuromuscular organization of feline anterior sartorius: I. Asymmetric distribution of motor units.

The neuromuscular organization of feline anterior sartorius was examined using three experimental approaches. First, the branching pattern of the nerve supplying anterior sartorius was inspected in muscles taken from a large number of feline cadavers. All muscles were found to be supplied by two major nerve branches, one directed proximally and the other directed distally, and most muscles (42/51) had a third distinct branch that entered the muscle centrally. Second, the motoneuronal populations supplying the three nerve branches were investigated by electrophysiological techniques. Motoneurons that supplied axons to the distally-directed branch did not appear to have collaterals in more proximally-located branches. In contrast, other motoneurons supplying the proximally-directed branch also appeared to supply axon collaterals to the centrally-directed branch. This result suggested that the motoneuronal population of the distally-directed branch was largely separate from that supplying the proximally- and centrally-directed branches. Third, the motor unit territories supplied by different nerve branches were mapped using glycogen-depletion methods. Muscle fibers supplied by the distally-directed nerve branch were mostly distributed to the medial portion of anterior sartorius, whereas the fibers supplied by the other two branches were generally found more anteriorly. Further, the muscle fibers supplied by an individual nerve branch were present in greater numbers at the end of the muscle closest to the entry point of that branch. Thus, the motor units supplied by discrete nerve branches were found to be distributed asymmetrically within anterior sartorius, but were arranged neither strictly in-parallel nor strictly in-series.

Adenosine Triphosphatases↗
PubMed1990

The anticonvulsant MK-801 interacts with peripheral and central nicotinic acetylcholine receptor ion channels.

The effects of MK-801 [( +]-5-methyl-10,11-dihydro-5H-di-benzo[a, d]cyclohepten-5,10-imine) on peripheral and central nicotinic receptors were studied using electrophysiological and biochemical techniques. MK-801 depressed the peak amplitude and accelerated the decay of end-plate currents. The drug (1-10 microM) decreased the frequency of activation of acetylcholine (ACh)-induced single-channel currents in addition to shortening the mean open and burst times of channels activated by either ACh or (+)anatoxin-a (AnTX). MK-801 (10-40 microM) depressed the single potentials and trains of ACh and AnTX-induced potentials in chronically denervated rat soleus muscles. MK-801 blocked the twitch responses (20-100 microM) of both frog sartorius and rat diaphragm muscles evoked by stimulation of their respective nerves. Also this drug (less than 1 microM) decreased the frequency of channels activated by AnTX or ACh in outside-out patch membranes of rat retinal ganglion cells with minimal changes in the channel open time. MK-801 (10-25 microM) depressed (-)nicotine-evoked gamma-amino[2,3-3H]butyric acid release from rat hippocampal synaptosomes; however, it failed to affect the binding of [3H](-)nicotine to brain membranes and also failed to interfere with the binding of [125I]alpha-bungarotoxin to either frog muscle or Torpedo membranes. On the other hand, MK-801 inhibited the binding of [3H]perhydrohistrionicotoxin to Torpedo membranes and such an effect was more pronounced in the presence of carbamylcholine. Neither AnTX nor any other nicotinic agonist increased the binding of [3H]MK-801 to the N-methyl-D-aspartate receptor ion channel complex. The actions of MK-801 were evident at concentrations comparable with those needed to block N-methyl-D-aspartate receptors. These results demonstrate the existence of at least three different types of nicotinic AChR, all of which were blocked noncompetitively by MK-801.

Acetylcholine↗
PubMed1992

Imaging techniques in myotonic dystrophy. A comparative study of ultrasound, computed tomography and magnetic resonance imaging of skeletal muscles.

Limb and trunk muscles of 57 patients with the juvenile or adult form of myotonic dystrophy were studied by imaging techniques (ultrasound, computed tomography, magnetic resonance imaging). Typical findings were atrophy of the tibialis anterior and triceps brachii muscles and fatty degeneration of the vastus intermedius, sartorius, tibialis anterior and soleus muscles as well as of medial head of the gastrocnemius muscle. Magnetic resonance imaging was the most sensitive technique in depicting mesenchymal muscle alterations, followed by computed tomography and ultrasound. The data support that imaging is more sensitive in detecting the myopathy than measurement of the creatine kinase activity.

Adolescent↗