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PubMed1992

Detection of motor unit action potentials with surface electrodes: influence of electrode size and spacing.

A model of the motor unit action potential was developed to investigate the amplitude and frequency spectrum contributions of motor units, located at various depths within muscle, to the surface detected electromyographic (EMG) signal. A dipole representation of the transmembrane current in a three-dimensional muscle volume was used to estimate detected individual muscle fiber action potentials. The effects of anisotropic muscle conductance, innervation zone location, propagation velocity, fiber length, electrode area, and electrode configuration were included in the fiber action potential model. A motor unit action potential was assumed to be the sum of the individual muscle fiber action potentials. A computational procedure, based on the notion of isopotential layers, was developed which substantially reduced the calculation time required to estimate motor unit action potentials. The simulations indicated that: 1) only those motor units with muscle fibers located within 10-12 mm of the electrodes would contribute significant signal energy to the surface EMG, 2) variation in surface area of electrodes has little effect on the detection depth of motor unit action potentials, 3) increased interelectrode spacing moderately increases detection depth, and 4) the frequency content of action potentials decreases steeply with increased electrode-motor unit territory distance.

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PubMed1987

Calcium channel components of action potential in chick skeletal muscle cells developing in culture.

The action potential was recorded from cultured chick skeletal muscle cells in Na-, Ca-, Cl-free saline containing Ba and tetraethylammonium ions (Ba saline). The action potential consisted of two components: a low-threshold, fast inactivating component and a high-threshold, long-lasting component. Both components of the action potential were dependent on external Ba ions and eliminated by Co ions. It is concluded that both components are generated by inward currents carried by Ba ions through Ca channels. The two Ca channel components of the action potential differed with regard to activation and inactivation potential, presence or absence of fast inactivation, sensitivity to an organic Ca channel blocker, and developmental profile. In addition, the failure of occurrence of one or the other components was observed in some cells. These results could be explained by assuming that two components of the action potential in Ba saline were mediated by the two different Ca channels. Furthermore, there was a tendency for younger cells to have more prominent Ca channel components. This may suggest that Ca channels have some function in the early stages of myogenesis.

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PubMed1998

Effects of troglitazone and pioglitazone on the action potentials and membrane currents of rabbit ventricular myocytes.

The effects of the antidiabetic thiazolidinediones troglitazone and pioglitazone on action potentials and membrane currents were studied in rabbit ventricular myocytes. Troglitazone (10 microM) reversibly reduced excitability of the myocytes and modified their action potential configuration. It significantly increased the stimulation threshold required to elicit action potentials and decreased action potential amplitude and the maximum upstroke velocity of the action potentials. The Inhibition of the maximum upstroke velocity by troglitazone was also significant at 1 microM. Voltage-clamp experiments revealed that troglitazone (10 microM) reversibly inhibited both the slow inward Ca2+ current and the steady-state K+ current. In contrast to troglitazone, pioglitazone (1-10 microM) had no significant effect on the excitability, action potential configuration, or membrane currents of myocytes. These results suggest that troglitazone, but not pioglitazone, modulates Na+, Ca2+ and K+ currents, leading to the changes in excitability and action potential configuration of ventricular myocytes.

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PubMed1975

The ionic dependence of action potentials induced by colchicine in an insect motoneurone cell body.

1. The ionic requirements of the action potential recorded in the cell of an identified cockroach (Periplaneta americana) motoneurone following pre-treatment of the animal with colchicine have been studied. 2. Small cubes of gelatin containing 1% colchicine were implanted into one metathoracic leg near to the nerve trunk containing the axon of the identified motoneurone. 3. Electrophysiological experiments were performed 4--10 days after this treatment, when action potentials which frequently overshoot zero potential can be recorded from the cell body. Such action potentials are not normally seen in untreated animals. 4. Sodium-free solution reversibly abolished the action potential within 5 min. 5. Tetrodotoxin (10(-8)M) reversibly depressed the action potential. It was totally abolished by 10(-7)M tetrodotoxin, but this effect was not reversible. 6. Saline solution containing 40 mM manganous chloride either had no effect on the action potential amplitude, or caused a slight increase. It also caused prolongation of the falling phase and loss of the after-hyperpolarization. These effects were all reversible. 7. It is concluded that sodium carries a major proportion of the inward current of the action potential in this neurone. Some calcium probably enters also, and may, at least in part, be responsible for triggering the delayed rise in potassium conductance during the action potential.

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PubMed2004

Differential action potentials and firing patterns in injured and uninjured small dorsal root ganglion neurons after nerve injury.

The profile of tetrodotoxin sensitive (TTX-S) and resistant (TTX-R) Na(+) channels and their contribution to action potentials and firing patterns were studied in isolated small dorsal root ganglion (DRG) neurons after L5/L6 spinal nerve ligation (SNL). Total TTX-R Na(+) currents and Na(v) 1.8 mRNA were reduced in injured L5 DRG neurons 14 days after SNL. In contrast, TTX-R Na(+)currents and Na(v) 1.8 mRNA were upregulated in uninjured L4 DRG neurons after SNL. Voltage-dependent inactivation of TTX-R Na(+) channels in these neurons was shifted to hyperpolarized potentials by 4 mV. Two types of neurons were identified in injured L5 DRG neurons after SNL. Type I neurons (57%) had significantly lower threshold but exhibited normal resting membrane potential (RMP) and action potential amplitude. Type II neurons (43%) had significantly smaller action potential amplitude but retained similar RMP and threshold to those from sham rats. None of the injured neurons could generate repetitive firing. In the presence of TTX, only 26% of injured neurons could generate action potentials that had smaller amplitude, higher threshold, and higher rheobase compared with sham rats. In contrast, action potentials and firing patterns in uninjured L4 DRG neurons after SNL, in the presence or absence of TTX, were not affected. These results suggest that TTX-R Na(+) channels play important roles in regulating action potentials and firing patterns in small DRG neurons and that downregulation in injured neurons and upregulation in uninjured neurons confer differential roles in shaping electrogenesis, and perhaps pain transmission, in these neurons.

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PubMed1972

The dependence of plateau currents in cardiac Purkinje fibres on the interval between action potentials.

1. The influence of diastolic interval on ionic currents that may determine the action potential duration in cardiac Purkinje fibres was investigated. As the diastolic interval is shortened from about 5 sec, the first effect on the action potential is to reduce and then abolish the notch at the beginning of the plateau.2. This effect corresponds to the influence of diastolic interval on the magnitude of a transient outward chloride current known as the ;dynamic current'.3. Further shortening of the diastolic interval produces a slight shortening of the action potential until intervals less than about 500 msec are used. The action potential then becomes considerably shorter. The ;time constant' of decay of this major influence of one action potential on the duration of the subsequent action potential is about 200 msec.4. This effect corresponds to the time course of decay of an outward (mainly K) current known as i(x1).5. It is shown that variations in the magnitude of i(x1) may be responsible for the alternation in action potential duration at the beginning of a train of stimuli known as ;electrical alternans'.6. The results in general are consistent with the view that i(x1) is the main current involved in determining the interval-duration relation although they cannot exclude the possibility that an inward current with a reavailability time course similar to the decay time course of i(x1) might also be involved.

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PubMed2006

Action-potential initiation and maintained activity of the isolated frog muscle spindle.

The initiation of afferent action potentials represents the basic signalling process integrating and coding information of an external stimulus. There is also evidence in sensory receptor neurons of spontaneously generating action potentials that interfere with and modify the stimulus evoked activity. The present study investigates the generation of spontaneous action potentials in the isolated muscle spindle of the frog by recording receptor potentials, small subthreshold depolarizations, propagated impulses and interspike transients from the first Ranvier-node of the afferent stem fibre. The temporal pattern of spontaneous discharges at resting length depended on several variables interacting at the encoding site. In the absence of mechanical stimulation, a large resting receptor potential steadily depolarized the encoding node and provoked action potentials at irregular intervals. After each action potential, the hyperpolarizing afterpotential provided a slowly increasing depolarizing interspike transient of decreasing slope (time constant 128 ms), which evoked small subthreshold depolarizations (decay time > 5 ms; multimodal amplitude distribution) before the following action potential discharged. The probability of the small subthreshold depolarizations increased the longer the resting receptor potential stayed constant at its maximum amplitude. When increasing the static prestretch level encoding depended also on the stretch-evoked receptor potential as an additional parameter. The resulting depolarizing interspike transients were then larger and also more steeply rising, so that the afferent discharges increased in both rate and regularity. The experiments show dynamic threshold patterns that control action-potential initiation by the assessment of the actual amplitude of depolarization and its rate of rise.

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PubMed1988

Does acute exposure to amiodarone prolong cardiac action potential duration?

1. The acute effects of a potent antiarrhythmic agent, amiodarone (AM), were studied in isolated guinea pig ventricular muscle. Transmembrane action potentials were recorded by conventional microelectrode techniques, and isometric contractile tension, by a strain gauge. 2. Short-term (30 min) exposure to 4.4 x 10(-5) M AM did not significantly effect action potential characteristics, whereas the peak developed tension was significantly depressed. 3. On the other hand, long-term (3-5 hr) exposure to the same concentration of AM led to a significant decrease in the resting membrane potential, amplitude of action potential, overshoot of action potential, maximum upstroke velocity of action potential, and the peak developed tension. However, the duration of action potential at all levels of repolarization was not significantly effected by 4.4 x 10(-5) M AM during the entire duration of the experiment. 4. These results suggest that the acute AM's antiarrhythmic actions reported may be not due to APD-lengthening action, but probably due to other actions (mainly, inhibition of Na+ channels, Ca2+ channels).

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PubMed1991

Differences in the effect of metabolic inhibition on action potentials and calcium currents in endocardial and epicardial cells.

BACKGROUND: Ischemia-induced electrophysiological changes are more prominent in epicardial cells than in endocardial cells. Epicardial action potentials shorten more than endocardial action potentials during ischemia. Since the L-type Ca2+ current plays an important role in the maintenance of action potential duration, we hypothesized that the Ca2+ current is affected more in epicardial cells than in endocardial cells during ischemia. METHODS AND RESULTS: To test this hypothesis, we examined the effect of metabolic inhibition, a major component of ischemia, on action potentials and the Ca2+ current in single cells isolated from the endocardial and epicardial layers of the feline left ventricle. The membrane voltage and current were measured by using the whole-cell mode of the patch-clamp technique. During control periods, action potentials recorded from epicardial myocytes had lower amplitude, a prominent notch between phases 1 and 2, and shorter action potential duration compared with those recorded from endocardial myocytes. However, the amplitude and current-voltage relation of the Ca2+ current were similar in endocardial and epicardial cells at test potentials of -30 to 60 mV elicited from a holding potential of -40 mV. The time course of inactivation of the Ca2+ current also was identical in the two cell types. After 15 minutes of superfusion with glucose-free Tyrode's solution containing 1 mM CN-, action potential duration was reduced by 13 +/- 7% in endocardial cells and by 80 +/- 9% in epicardial cells (p less than 0.01). The peak Ca2+ current was reduced by 21 +/- 9% in endocardial cells and by 37 +/- 6% in epicardial cells (p less than 0.01). CONCLUSIONS: We conclude that enhanced depression of the Ca2+ current may account in part for the greater action potential shortening in epicardial cells during ischemia and metabolic inhibition.

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PubMed1996

Effect of a prenylamine analog (MG8926) on spontaneous action potentials in isolated rabbit sinoatrial node.

Effects of verapamil, prenylamine and a prenylamine analog, MG8926 on the intracellular spontaneous action potentials recorded from the isolated rabbit sinoatrial (SA) node were studied. Verapamil (1 microM), a selective inhibitor for slow Ca2+ channels, prolonged the cycle length, decreased the rate of diastolic depolarization, the rate of rise of action potential, the amplitude of action potential and the maximal diastolic potential, and usually arrested showing subthreshold fluctuation of the membrane potential within several ten min. Prenylamine (10 microM), a nonselective inhibitor for slow Ca2+ channels, tended to prolong the cycle length to decrease the diastolic depolarization, the rate of rise of action potential, the amplitude of action potential. However, these changes were statistically insignificant. Prenylamine at the concentration of 10 microM had no effect on the maximal diastolic potential. MG8926 (10 microM) prolonged the cycle length, decreased the rate of diastolic depolarization, the rate of rise of action potential and tended to decrease the amplitude of action potential. MG8926 at the concentration of 10 microM had almost no effect on the maximal diastolic potential. The present findings may indicate that replacement of phenyl residue of prenylamine by cyclohexyl residue increases the inhibitory action on the slow Ca2+ channels in rabbit SA node.

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PubMed1981

Serial action potential analysis in Guillain-Barré syndrome.

Action potential analyses were carried out in 62 skeletal muscles of 16 patients with the Guillain-Barré syndrome. The muscles of a good prognosis showed only a slight change in duration, amplitude and phase of action potentials on electromyograms. On the other hand, the muscles of a poor prognosis showed a marked increase in duration and amplitude of action potentials, especially in the chronic stage. The incidence of polyphasic potentials was more frequent in the early stage than in the chronic stage of the muscles of a poor prognosis. The changes in duration in the early stage of a poor prognosis muscles were similar to those of acute beriberi neuropathy and the changes in the later stage were similar to those of amyotrophic lateral sclerosis, both of which showed axonal degenerations. In the early stage, myopathy-like changes in electromyography were often noticed, but the muscle biopsy showed only early neurogenic changes. Coupling or satellite discharges were found most frequently six or eight months after the onset, and decreased in number in the chronic stage. Satellites with blockings appeared earlier than those without blockings. A poor prognosis might be induced by an axonal degeneration partly together with segmental demyelinations.

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PubMed1996

Pharmacologic alterations in human type I atrial flutter cycle length and monophasic action potential duration. Evidence of a fully excitable gap in the reentrant circuit.

OBJECTIVES: This study compared the effect of changes in action potential duration versus conduction velocity on atrial flutter cycle length to determine whether there is a fully or partially excitable gap in atrial flutter. BACKGROUND: In an excitable gap reentrant circuit, cycle length is proportional to conduction velocity. Action potential duration is not a direct determinant of cycle length when the gap is fully excitable. METHODS: Right atrial monophasic action potentials were recorded from 41 patients during type I atrial flutter before and during pharmacologic interventions. RESULTS: Adenosine (17 +/- 3 mg [mean +/- SD]) shortened (p < 0.001) action potential duration but did not change cycle length. Edrophonium (10 mg) had no significant effect on action potential duration or cycle length. Isoproterenol (0.03 microgram/kg body weight per min) shortened (p < 0.05) and procainamide (15 mg/kg, then 2 mg/min) prolonged (p < 0.001) action potential duration and cycle length. Alterations in cycle length were not correlated with changes in action potential duration. Procainamide's prolongation of action potential duration was reversed by adenosine without affecting cycle length. Procainamide's prolongation of action potential duration and cycle length was partially reversed by isoproterenol. Adenosine's and isoproterenol's shortening of action potential duration and isoproterenol's shortening of cycle length were enhanced by procainamide. CONCLUSIONS: Atrial flutter cycle length is determined primarily by conduction velocity and does not depend directly on action potential duration. Atrial flutter has a fully excitable gap, and procainamide does not convert the gap from full to partial excitability. Adenosine and isoproterenol interact with procainamide such that their effects are enhanced and procainamide's effects are diminished.

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PubMed1986

Repetitive action potentials induced in chloride-free solution: effect of denervation.

Isometric mechanical activity and action potentials registered with intracellular microelectrodes were studied in innervated and denervated fibers of the soleus muscle of the rat in normal and chloride-free solutions. The chloride-free solution promoted in both innervated and denervated fibers an increment in the resting membrane potential. The innervated muscles showed long mechanical relaxation and repetitive action potentials after a single depolarizing pulse. On the contrary, denervated muscles were resistant to show mechanical and electrical changes in the chloride-free medium. Spontaneous and evoked action potentials from innervated muscle fibers were abolished by tetrodotoxin. The evoked action potentials generated in denervated fibers had a slower time course and were resistant to tetrodotoxin. After 7 to 10 days of denervation the input resistance was increased by about 30%. Substitution of chloride with sulfate resulted in a 150% increase in input resistance of innervated muscle fibers and 80% in denervated preparations. Alterations in the ionic conductances, a decrease in the maximum rate of rise of the action potentials, and changes in the sodium current kinetics could be the main factors for the absence of repetitive action potentials in denervated fibers exposed to the chloride-free medium.

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PubMed1982

Effects of L-carnitine on action potential or canine papillary muscle impaired by long chain acyl carnitine.

It has been reported that long chain acyl carnitine accumulates in ischemic myocardium, and L-carnitine prevents ventricular arrhythmias as well as the accumulation of long chain acyl carnitine in ischemic and free fatty acid supplemented hearts. The purpose of this study was to observe the electrophysiological effects of long chain acyl carnitine, and to evaluate the protective effect of L-carnitine on the transmembrane action potential impaired by long chain acyl carnitine. Using standard microelectrode techniques, transmembrane action potentials were recorded from isolated canine papillary muscle. Palmitoyl carnitine (0.3 mM and 0.6 mM) decreased the resting membrane potential, action potential amplitude and maximum upstroke velocity of phase 0, and shortened action potential duration and effective refractory period in a concentration-dependent manner. Application of L-carnitine (25 mM) prevented the effect of palmitoyl carnitine (0.3 mM) on the transmembrane action potential. These results suggest that long chain acyl carnitine plays an important role in arrhythmogenesis, and that the effect is prevented by L-carnitine.

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PubMed1989

Simultaneous measurements of action potential duration and intracellular ATP in isolated ferret hearts exposed to cyanide.

Shortening of the cardiac action potential during ischemia and anoxia is likely to contribute to the decline in contractility that occurs under such conditions. It has been hypothesized that a decrease in the intracellular ATP concentration ([ATP]i) underlies the changes in the action potential. The recently discovered potassium channel activated at low ATP concentrations might provide the link between action potential shortening and low [ATP]i. However, it has yet to be shown that [ATP]i falls to the range required for channel activation at the time when action potential shortening occurs. We have measured action potentials and [ATP]i simultaneously in isolated ferret hearts during inhibition of both oxidative phosphorylation and anaerobic glycolysis (metabolic blockade). Metabolic blockade caused a rapid decline in cardiac contractility, accompanied by a rapid fall in action potential duration. [ATP]i fell only slightly and remained well above the range where activation of the ATP-sensitive K+ channel would be expected to occur. Moreover, reintroduction of glucose to the perfusate led to a substantial recovery in both contraction and in action potential duration, again in the absence of any great change in [ATP]i. These results suggest that the action potential shortening observed in metabolic blockade cannot be explained by the simple hypothesis of K+ channel opening as a consequence of a decrease in bulk [ATP]i unless the Km for suppression of channel activity by ATP is very much higher in intact cells than in any of the patch configurations studied. An alternative explanation is that the channel may be regulated under these conditions by mechanisms other than a change in [ATP]i.

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PubMed1993

Failure to generate action potentials in newborn diaphragms following nerve stimulation.

Action potentials were recorded intracellularly from single diaphragmatic fibers, in vitro, of newborn (3-10 d, n = 18) and older (> or = 21 d, n = 10) rats using flexible microelectrodes. At 20 and 50 Hz phrenic nerve stimulation (1 s duration), action potential transmission failure was significantly higher in the newborn than in the older fibers. During the failure periods, small and highly variable depolarizations were observed which were most likely EPPs. These results show that failure of action potential transmission across the neuromuscular junction is more prevalent in the newborn, and we speculate that this failure is due to inadequate release of neurotransmitter in newborn muscle fibers.

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PubMed1990

Angiotensin stimulates Ca2(+)-dependent action potentials in cultured smooth muscle cells.

The steady-state angiotensin II response was measured in primary cultures of reaggregated vascular smooth muscle cells derived from rat aorta by use of intracellular microelectrode recording of membrane potentials. Angiotensin II (10(-9)-10(-6) M) produced a depolarization which triggered a single action potential, consisting of a spike plus plateau. In addition, angiotensin II prolonged the action potential plateau and lowered input resistance. The angiotensin II-induced action potentials and the action potential plateau prolongation were inhibited by verapamil. Saralasin blocked the occurrence of angiotensin II-induced action potentials and reversed the increase in action potential duration provoked by angiotensin II. Saralasin, in the absence of angiotensin II, exhibited agonistic activity which was manifest by plateau prolongation. Therefore, angiotensin II, through interaction of the peptide with its receptor, depolarizes cultured vascular smooth muscle cells and prolongs the calcium-dependent action potentials. These effects could be mediated by the known ability of angiotensin II to stimulate production of inositol trisphosphate and diacylglycerol, and activation of protein kinase C.

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PubMed1992

Potassium currents contributing to action potential repolarization and the afterhyperpolarization in rat vagal motoneurons.

1. Intracellular recordings were made from neurons in the dorsal motor nucleus of the vagus (DMV) in transverse slices of rat medulla maintained in vitro at 30 degrees C. Neurons had a resting potential of -59.8 +/- 1.4 (SE) mV (n = 39) and input resistance of 293 +/- 23 M omega (n = 44). 2. Depolarization elicited overshooting action potentials that were blocked by tetrodotoxin (TTX; 1 microM). In the presence of TTX, two types of action potentials having low and high thresholds could be elicited. The action potentials were blocked by cobalt (2 mM) indicating they were mediated by calcium currents. 3. Under voltage clamp, depolarization of the cell from membrane potentials negative of the resting potential activated a transient potassium current. This current was selectively blocked by 4-aminopyridine (4-AP) (5 mM) and catechol (5 mM) indicating that it is an A-type current. This current inactivated with a time constant of 420 ms and recovered from inactivation with a time constant of 26 ms. 4. When calcium currents were blocked by cadmium or cobalt, the rate of action potential repolarization was slower. In the presence of tetraethylammonium (TEA; 200-400 microM) or charybdotoxin (CTX; 30 nM) a small "hump" appeared on the repolarizing phase of the action potential that was abolished by addition of cadmium. These results indicate that a calcium-activated potassium current (IC) contributes to action potential repolarization. 5. Actions potentials elicited from hyperpolarized membrane potentials repolarized faster than those elicited from resting membrane potential. This effect could be blocked by catechol, indicating that voltage-dependent potassium currents (IA) can also contribute to action-potential repolarization. In the presence of catechol and calcium channel blockers, action potentials still had a significant early afterhyperpolarization suggesting that another calcium independent outward current is also active during repolarization. This fast afterhyperpolarizations (AHP) was not blocked by TEA. 6. Action potentials were followed by prolonged AHPs, which had two phases. The initial part of the AHP was blocked by apamin (100 nM) indicating that it results from activation of SK type calcium-activated potassium channels. The slow phase was selectively blocked by catechol suggesting that it is due to activation of IA. 7. It is concluded that a TTX-sensitive sodium current and two calcium currents contribute to the action potential in rat DMV neurons. At least three different currents contribute to action-potential repolarization: IC, IA, and a third unidentified calcium-insensitive outward current.(ABSTRACT TRUNCATED AT 400 WORDS)

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