scholarly journals Double Sucrose-Gap Method Applied to Single Muscle Fiber of Xenopus laevis

1974 ◽  
Vol 63 (2) ◽  
pp. 235-256 ◽  
Author(s):  
Shigehiro Nakajima ◽  
Joseph Bastian
Keyword(s):  
Electrical Properties ◽  
Action Potential ◽  
Muscle Fiber ◽  
Time Course ◽  
Muscle Fibers ◽  
Membrane Conductance ◽  
Frog Muscle ◽  
Muscle Twitch ◽  
Sucrose Gap ◽  
Isotonic Shortening

Passive electrical properties (internal conductance, membrane conductance, low frequency capacity, and high frequency capacity obtained from the foot of the action potential) of normal and glycerol-treated muscle of Xenopus were determined with the intracellular microelectrode technique. The results show that the electrical properties of Xenopus muscle are essentially the same as those of frog muscle. Characteristics of the action potential of Xenopus muscle were also similar to those of frog muscle. Twitch tension of glycerol-treated muscle fibers of Xenopus recovered partially when left in normal Ringer for a long time (more than 6 h). Along with the twitch recovery, the membrane capacity increased. Single isolated muscle fibers of Xenopus were subjected to the double sucrose-gap technique. Action potentials under the sucrose gap were not very different from those obtained with the intracellular electrode, except for the sucrose-gap hyperpolarization and a slight tendency toward prolongation of the shape of action potential. Twitch contraction of the artificial node was recorded as a change of force from one end of the fiber under the sucrose gap. From the time-course of the recorded force and the sinusoidal stress-strain relationship at varying frequencies of the resting muscle fiber, the time-course of isotonic shortening of the node was recovered by using Fourier analysis. It was revealed that the recorded twitch force can approximately be regarded as isotonic shortening of the node.

Inhibition of Zn2+-induced potentiation of twitch tension by Ni2+ in frog muscle

1986 ◽  
Vol 64 (5) ◽  
pp. 625-630
Author(s):  
Toshiharu Oba ◽  
Ken Hotta
Keyword(s):  
Action Potential ◽  
Inhibitory Action ◽  
Channel Blocker ◽  
Rana Catesbeiana ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Duration Of Action ◽  
Ringer’S Solution ◽  
Mechanical Threshold ◽  
T Tubules

Effect of Ni2+ on Zn2+-induced potentiation of twitch tension was studied electrophysiologically in the toe muscle fibers of Rana catesbeiana. The major findings of this investigation are as follows. When 2 mM Ni2+ was applied to fibers in a normal Ringer's solution containing 50 μM Zn2+ (Zn2+ solution), the Zn2+-potentiated twitch tension decreased remarkably to about one-third of that before Ni2+ treatment. This concentration of Ni2+ caused a 23% decrease in the duration of action potential which had been prolonged by Zn2+ (6.61–5.09 ms). Ni2+ (2 mM) added to normal Ringer's solution led to increases of about 30 and 42% in twitch tension and in the duration of action potential, respectively. A slight increase in the mechanical threshold was induced by 2 mM Ni2+. The inhibitory action of Ni2+ on the twitch tension in Zn2+ solution was larger than that in the case of tetanus tension. Diltiazem (40 μM), aCa2+ channel blocker, did not inhibit the twitch tension potentiated in Zn2+ solution. These results suggest that the decrease in Zn2+-potentiated twitch tension by Ni2+ may possibly derive from impairment of the propagation of action potential along the T tubules.

scholarly journals Ultraslow contractile inactivation in frog skeletal muscle fibers.

1990 ◽  
Vol 96 (1) ◽  
pp. 47-56 ◽  
Author(s):  
C Caputo ◽  
P Bolaños
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Muscle Fibers ◽  
Membrane Depolarization ◽  
Frog Muscle ◽  
Slow Time ◽  
Inactivation Curve ◽  
Lanthanum Ions ◽  
Skeletal Muscle Fibers ◽  
Spontaneous Relaxation

After a contracture response, skeletal muscle fibers enter into a state of contractile refractoriness or inactivation. Contractile inactivation starts soon after membrane depolarization, and causes spontaneous relaxation from the contracture response. Here we demonstrate that contractile inactivation continues to develop for tens of seconds if the membrane remains in a depolarized state. We have studied this phenomenon using short (1.5 mm) frog muscle fibers dissected from the Lumbricalis brevis muscles of the frog, with a two-microelectrode voltage-clamp technique. After a contracture caused by membrane depolarization to 0 mV, from a holding potential of -100 mV, a second contracture can be developed only if the membrane is repolarized beyond a determined potential value for a certain period of time. We have used a repriming protocol of 1 or 2 s at -100 mV. After this repriming period a fiber, if depolarized again to 0 mV, may develop a second contracture, whose magnitude and time course will depend on the duration of the period during which the fiber was maintained at 0 mV before the repriming process. With this procedure it is possible to demonstrate that the inactivation process builds up with a very slow time course, with a half time of approximately 35 s and completion in greater than 100 s. After prolonged depolarizations (greater than 100 s), the repriming time course is slower and the inactivation curve (obtained by plotting the extent of repriming against the repriming membrane potential) is shifted toward more negative potentials by greater than 30 mV when compared with similar curves obtained after shorter depolarizing periods (10-30 s). These results indicate that important changes occur in the physical state of the molecular moiety that is responsible for the inactivation phenomenon. The shift of the inactivation curve can be partially reversed by a low concentration (50 microM) of lanthanum ions. In the presence of 0.5 mM caffeine, larger responses can be obtained even after prolonged depolarization periods, indicating that the fibers maintain their capacity to liberate calcium.

Properties of self-reinnervated motor units of medial gastrocnemius of cat. II. Axotomized motoneurons and time course of recovery

1986 ◽  
Vol 55 (5) ◽  
pp. 947-965 ◽  
Author(s):  
R. C. Foehring ◽  
G. W. Sypert ◽  
J. B. Munson
Keyword(s):  
Electrical Properties ◽  
Motor Unit ◽  
Fatigue Resistance ◽  
Time Course ◽  
Muscle Fibers ◽  
Motor Units ◽  
Input Resistance ◽  
Medial Gastrocnemius ◽  
Muscle Properties ◽  
Fast Twitch

This study tested the hypothesis that functional connection to muscle is necessary for expression of normal motoneuron electrical properties. Also examined was the time course of self-reinnervation. Properties of individual medial gastrocnemius (MG) motor units were examined following section and reanastomosis of the MG nerve. Stages examined were 3-5 wk (prior to reinnervation, no-re), 5-6 wk (low-re), 9-10 wk (med-re), and 9 mo (long-re, preceding paper) after nerve section. Motor units were classified on the basis of their mechanical response as type fast twitch, fast fatiguing (FF), fast twitch with intermediate fatigue resistance (FI), fast twitch, fatigue resistant (FR), or slow twitch, fatigue resistant (S) (11, 24). Motoneuron electrical properties were measured. Muscle fibers were classified using histochemical methods as type fast glycolytic (FG), fast oxidative glycolytic (FOG), or slow oxidative (SO) (60). Prior to functional reinnervation, MG motoneurons exhibited increased input resistance, decreased rheobase, decreased rheobase/input resistance, and decreased axonal conduction velocity. There was no change in mean afterhyperpolarization (AHP) half-decay time. Normal relationships between motoneuron electrical properties were lost. These data are consistent with dedifferentiation of motoneuron properties following axotomy (35, 47). At 5-6 wk after reanastomosis, motor-unit tensions were small, and motoneuron membrane electrical properties were unchanged from the no-re stage. There were no differences in motoneuron electrical properties between cells that elicited muscle contraction and those that did not. Motor-unit types were first recognizable at the med-re stage. The proportions of fast and slow motor units were similar to normal MG. Within the fast units, there were fewer type-FF units and more type-FI and type-FR units than normal, reflecting a general increase in fatigue resistance at this stage. Neither motoneuron membrane electrical properties nor muscle contractile properties had reached normal values, although both were changed in that direction from the low-re stage. Normal relationships between muscle properties, between motoneuron properties, and between motoneuron and muscle properties were re-established. The correspondence between motor-unit type and motoneuron type was similar to normal or 9 mo reinnervated MG. Muscle-unit tetanic tensions became larger with time after reinnervation. Most of the increase in muscle tension beyond the med-re stage could be accounted for by increase in muscle fiber area. There was an increased proportion of SO muscle fibers observed in the med-re muscles, as at the long-re stage.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Capacitance of the Surface and Transverse Tubular Membrane of Frog Sartorius Muscle Fibers

1969 ◽  
Vol 53 (3) ◽  
pp. 265-278 ◽  
Author(s):  
Peter W. Gage ◽  
Robert S. Eisenberg
Keyword(s):  
Electrical Properties ◽  
Time Course ◽  
Muscle Fibers ◽  
Membrane Resistance ◽  
Ringer Solution ◽  
Sartorius Muscle ◽  
Tubular Membrane ◽  
Essentially Normal ◽  
The Difference ◽  
Passive Electrical Properties

The passive electrical properties of glycerol-treated muscle fibers, which have virtually no transverse tubules, were determined. Current was passed through one intracellular microelectrode and the time course and spatial distribution of the resulting potential displacement measured with another. The results were analyzed by using conventional cable equations. The membrane resistance of fibers without tubules was 3759 ± 331 ohm-cm2 and the internal resistivity 192 ohm-cm. Both these figures are essentially the same as those found in normal muscle fibers. The capacitance of the fibers without tubules is strikingly smaller than normal, being 2.24 ± 0.14 µF/cm2. Measurements were also made of the passive electrical properties of fibers in a Ringer solution containing 400 mM glycerol (which is used in the preparation of glycerol-treated fibers). The membrane resistance and capacitance are essentially normal, but the internal resistivity is somewhat reduced. These results show that glycerol in this concentration does not directly affect the membrane capacitance. Thus, the figure for the capacitance of glycerol-treated fibers, which agrees well with previous estimates made by different techniques, represents the capacitance of the outer membrane of the fiber. Estimates of the capacitance per unit area of the tubular membrane are made and the significance of the difference between the figures for the capacitance of the surface and tubular membrane is discussed.

The interactive effects of fatigue and pH on the ionic conductance of frog sartorius muscle fibers

1985 ◽  
Vol 63 (11) ◽  
pp. 1444-1453 ◽  
Author(s):  
J. M. Renaud ◽  
G. W. Mainwood
Keyword(s):  
Action Potential ◽  
Normal Values ◽  
Muscle Fibers ◽  
Membrane Conductance ◽  
Interactive Effects ◽  
Resting Potential ◽  
Sartorius Muscle ◽  
Ionic Conductance ◽  
Frog Sartorius Muscle ◽  
Frog Sartorius

The effects of fatigue on the membrane conductance of frog sartorius muscle at the resting potential and during an action potential were studied. When muscles were exposed to an extracellular pH of 8.0 the membrane conductance at the resting potential increased during fatigue by about 20% and returned to prefatigue level in about 20 min. The membrane conductance of muscle fibers exposed to pH 6.4 was about three times less than that of pH 8.0 and decreased further during fatigue. Furthermore, the recovery of a normal membrane conductance was slow at pH 6.4. Both the inward, depolarizing and the outward, repolarizing currents during the action potential are reduced in fatigue. In each case the effect is greater at pH 6.4 than at 8.0 and recovery towards normal values is slower at pH 6.4. It is concluded that the ionic conductance of the sareolemmal membrane at the resting potential and during an action potential are modified by fatigue and that these changes are modulated by pHo.

Stabilization and rectification of muscle fiber membrane by tetrodotoxin

1960 ◽  
Vol 198 (5) ◽  
pp. 934-938 ◽  
Author(s):  
Toshio Narahashi ◽  
Takehiko Deguchi ◽  
Norimoto Urakawa ◽  
Yoshio Ohkubo
Keyword(s):  
Muscle Fiber ◽  
Muscle Fibers ◽  
Membrane Resistance ◽  
Frog Muscle ◽  
Resting Potential ◽  
Fiber Membrane ◽  
Delayed Rectification ◽  
Intracellular Microelectrodes ◽  
Cathodal Current ◽  
Muscle Fiber Membrane

The mode of action of tetrodotoxin on the frog muscle fiber membrane has been analyzed with the aid of intracellular microelectrodes. Tetrodotoxin of 10–7 concentration made the applied cathodal current ineffective in producing action potential, whereas the resting potential and resting membrane resistance underwent little or no change. With 10–8 tetrodotoxin the muscle fibers responded with the small action potentials at high critical depolarizations. These results can be explained on the basis of the membrane being stabilized by inactivation of the sodium-carrying mechanism. Although delayed rectification was not observed in normal muscle fibers, it became apparent in the fibers rendered inexcitable by tetrodotoxin. This finding, together with other evidence in the existing literature, supports an applicability of the sodium theory to the frog muscle fibers.

Electrical properties of oxytocin neurons in organotypic cultures from postnatal rat hypothalamus

1996 ◽  
Vol 76 (4) ◽  
pp. 2772-2785 ◽  
Author(s):  
P. Jourdain ◽  
D. A. Poulain ◽  
D. T. Theodosis ◽  
J. M. Israel
Keyword(s):  
Electrical Properties ◽  
Action Potential ◽  
Glutamate Receptors ◽  
Action Potentials ◽  
Firing Pattern ◽  
Membrane Conductance ◽  
Input Resistance ◽  
Resting Potential ◽  
Organotypic Cultures ◽  
Current Pulses

1. Intracellular recordings were performed on immunocytochemically identified oxytocin (OT) neurons (n = 101) maintained for 2-7 wk in hypothalamic organotypic cultures derived from 4-to 6-day-old rat neonates. The neurons displayed a resting potential of -58.9 +/- 6.8 mV (mean +/- SD, n = 74), an input resistance of 114 +/- 26.8 M omega (n = 66), and a time constant of 9.6 +/- 1.4 ms (n = 57). Voltage-current (V-I) relations, linear at resting potential, showed a pronounced outward rectification when depolarized from hyperpolarized membrane potentials. At these hyperpolarized potentials, depolarizing current pulses induced a delayed action potential. 2. Action potentials had an amplitude of 73.4 +/- 9.7 mV and a duration of 1.9 +/- 0.2 ms. Each action potential was followed by an afterhyperpolarization of 7.9 +/- 2.0 mV in amplitude lasting 61.7 +/- 11.3 ms. The depolarizing phase of action potentials was both Na+ and Ca2+ dependent, whereas repolarization was due to a K+ conductance increase. 3. When Ba2+ was substituted for Ca2+ in the medium, OT neurons displayed prolonged sustained depolarizations. In the presence of tetrodotoxin (TTX), these depolarizations were triggered by depolarizing current pulses and arrested by hyperpolarizing current pulses or by local application of Ca2+, Co2+, Cd2+, No sustained depolarization was obtained when nifedipine was added to the medium. These data suggest that OT cells in organotypic culture possess L-type Ca2+ channels. 4. All OT neurons generated spontaneous action potentials at resting potential. Of 59 neurons, 29 showed a slow, irregular firing pattern (< or = 2.5 spikes/s), 24 generated a fast continuous firing pattern (> or = 2.5 spikes/s), and 6 cells displayed a bursting pattern of activity consisting of alternating periods of spike discharge and quiescence. None of the bursting cells exhibited regenerative endogenous potentials (plateau potentials). On the contrary, in four of these cells, the bursting activity was clearly due to patterned synaptic activity. 5. The cultured OT cells responded to exogenous gamma-aminobutyric acid (GABA) and muscimol with a hyperpolarization and an increase in membrane conductance. These effects still were observed in the presence of TTX, indicating that they were due to direct activation of GABA receptors in the cells. The GABA-induced response was mediated by GABAA receptors because it was blocked by bicuculline, but not by GABAB receptors, because baclofen and hydroxysaclofen had no effect on membrane potential and input resistance. 6. OT neurons responded to exogenous glutamate, quisqualate, and kainate with a depolarization concomitant with an increase in membrane conductance. N-methyl-D-aspartate depolarized the cells in Mg(2+)-free medium. These effects were observed in the presence of TTX, suggesting that OT cells expressed ionotropic glutamate receptors. Trans-(1S,3R)-1-amino-1,3-cyclopentane-dicarboxylic acid and (+/-)-alpha-amino-4-carboxymethylphenylglycine had no effect on OT cells, thus excluding the presence of metabotropic glutamate receptors. 7. Taken together, our observations demonstrate that hypothalamic slice cultures from 4- to 6-day-old rat neonates contain well-differentiated OT neurons that display electrical properties similar to those shown by adult neurons in vitro. Such cultures provide a reliable model to investigate membrane properties of adult OT neurons and a useful means to study the long-term modulation of their electrical behaviour by various agents known to affect OT cells in vivo.

Cellular mechanisms of fatigue in skeletal muscle

1991 ◽  
Vol 261 (4) ◽  
pp. 1-1 ◽  
Author(s):  
H. Westerblad ◽  
J. A. Lee ◽  
J. Läuml;nnergren ◽  
D. G. Allen
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Creatine Phosphokinase ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Cellular Mechanisms ◽  
Left Hand ◽  
Hand Column ◽  
Right Hand ◽  
On Line

Pages C195–C209: H. Westerblad, J. A. Lee, J. Lännergren, and D. G. Allen. “Cellular mechanisms of fatigue in skeletal muscle.” Page C198, left-hand column, paragraph 2, sentence beginning on line 15 should read: If the creatine phosphokinase reaction is assumed to be at equilibrium, a calculation of free ADP reveals an increase from ≈30 to 200 μM (27). Page C198, right-hand column, paragraph 3, sentence beginning on line 3 should read: From measurements in frog muscle fibers it has been calculated that for each action potential there would be an increase in the intracellular Na+ concentration ([Na+]i) of ≈7.7 μM and a decrease of the intracellular K+ concentration ([K+]i) of ap4.7 μM (52).

scholarly journals Comparison of regulated passive membrane conductance in action potential–firing fast- and slow-twitch muscle

2009 ◽  
Vol 134 (4) ◽  
pp. 323-337 ◽  
Author(s):  
Thomas Holm Pedersen ◽  
William Alexander Macdonald ◽  
Frank Vincenzo de Paoli ◽  
Iman Singh Gurung ◽  
Ole Bækgaard Nielsen
Keyword(s):  
Action Potential ◽  
Muscle Fibers ◽  
Membrane Conductance ◽  
Fiber Types ◽  
Channel Inhibition ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch ◽  
Passive Membrane

In several pathological and experimental conditions, the passive membrane conductance of muscle fibers (Gm) and their excitability are inversely related. Despite this capacity of Gm to determine muscle excitability, its regulation in active muscle fibers is largely unexplored. In this issue, our previous study (Pedersen et al. 2009. J. Gen. Physiol. doi:10.1085/jgp.200910291) established a technique with which biphasic regulation of Gm in action potential (AP)-firing fast-twitch fibers of rat extensor digitorum longus muscles was identified and characterized with temporal resolution of seconds. This showed that AP firing initially reduced Gm via ClC-1 channel inhibition but after ∼1,800 APs, Gm rose substantially, causing AP excitation failure. This late increase of Gm reflected activation of ClC-1 and KATP channels. The present study has explored regulation of Gm in AP-firing slow-twitch fibers of soleus muscle and compared it to Gm dynamics in fast-twitch fibers. It further explored aspects of the cellular signaling that conveyed regulation of Gm in AP-firing fibers. Thus, in both fiber types, AP firing first triggered protein kinase C (PKC)-dependent ClC-1 channel inhibition that reduced Gm by ∼50%. Experiments with dantrolene showed that AP-triggered SR Ca2+ release activated this PKC-mediated ClC-1 channel inhibition that was associated with reduced rheobase current and improved function of depolarized muscles, indicating that the reduced Gm enhanced muscle fiber excitability. In fast-twitch fibers, the late rise in Gm was accelerated by glucose-free conditions, whereas it was postponed when intermittent resting periods were introduced during AP firing. Remarkably, elevation of Gm was never encountered in AP-firing slow-twitch fibers, even after 15,000 APs. These observations implicate metabolic depression in the elevation of Gm in AP-firing fast-twitch fibers. It is concluded that regulation of Gm is a general phenomenon in AP-firing muscle, and that differences in Gm regulation may contribute to the different phenotypes of fast- and slow-twitch muscle.

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