ACTION OF ETHER ON FROG SKELETAL MUSCLE

1965 ◽  
Vol 43 (5) ◽  
pp. 751-761 ◽  
Author(s):  
F. Inoue ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Electrical Activity ◽  
Effective Resistance ◽  
Frog Skeletal Muscle ◽  
Sodium Conductance ◽  
Low Concentrations ◽  
Adequate Stimulus ◽  
Specific Increase ◽  
Microelectrode Techniques

The mechanisms for the excitability changes produced by ether on the electrical activity of frog skeletal muscle were investigated by intracellular microelectrode techniques. Low concentrations of ether (less than 1%) increased excitability by increasing the 'effective resistance' between the inside and the outside of the fiber at the point of stimulation, thereby reducing the current needed to initiate an action potential. Higher concentrations decreased excitability by inhibiting the specific increase in sodium conductance which normally follows an adequate stimulus and is responsible for the rising phase of the action potential.

Effects of Morphine and Meperidine on Action Potential Production in Frog's Skeletal Muscle Fibers

1975 ◽  
Vol 53 (1) ◽  
pp. 92-96 ◽  
Author(s):  
G. B. Frank ◽  
H. S. Buttar
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Action Potential Duration ◽  
Muscle Fibers ◽  
Potassium Conductance ◽  
Potential Production ◽  
Skeletal Muscle Fibers ◽  
Adequate Stimulus ◽  
Specific Increase ◽  
Secondary Rise

Morphine (3.3 × 10−4–33 × 10−4 M) and meperidine (8.8 × 10−5–35 × 10−5 M) inhibited action potential production in frog's skeletal muscle fibers. Over these concentration ranges, neither the resting membrane potentials nor the resting membrane electric properties of the fibers appeared to be modified. Both drugs depressed excitability and the rising phase of the action potential by inhibiting the specific increase in sodium conductance which normally follows an adequate stimulus. Both drugs also seemed to inhibit the secondary rise in potassium conductance which normally occurs during an action potential, causing a prolongation of the action potential duration.

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

An investigation of the activity of opiate drug receptors located on frog skeletal muscle fibre membrane

1978 ◽  
Vol 56 (3) ◽  
pp. 501-508 ◽  
Author(s):  
G. B. Frank ◽  
J. Marwaha
Keyword(s):  
Skeletal Muscle ◽  
Action Potentials ◽  
Skeletal Muscle Fibre ◽  
Second Phase ◽  
Frog Skeletal Muscle ◽  
Potential Production ◽  
Low Concentrations ◽  
Drug Receptors ◽  
Frog Sartorius ◽  
Opiate Drug

Extracellular and intracellular microelcctrode studies were conducted to test the actions and interactions of opiate agonists, antagonists, and procaine on action potentials in frog sartorius muscles. Extracellular studies showed that morphine, methadone, propoxyphene, and procaine all depressed action potential production. Low concentrations of naloxone or naltrexone antagonized the excitability depression produced by the three opiate agonists but not the depression produced by procaine. Intracellular studies revealed that certain concentrations of the opiate agonists produced a biphasic decline in the stimulus-induced increase in sodium conductance (gNa). Naloxone or naltrexone antagonized only the second phase of this decline. These results show that part of the excitability depression produced by opiate agonists is due to an action on opiate drug receptors.

scholarly journals Differential effects of tetracaine on charge movements and Ca2+ signals in frog skeletal muscle.

1988 ◽  
Vol 92 (5) ◽  
pp. 601-612 ◽  
Author(s):  
L Csernoch ◽  
C L Huang ◽  
G Szucs ◽  
L Kovacs
Keyword(s):  
Skeletal Muscle ◽  
Charge Transfer ◽  
Calcium Release ◽  
Charge Movement ◽  
Frog Skeletal Muscle ◽  
Semitendinosus Muscle ◽  
Contraction Coupling ◽  
Low Concentrations ◽  
Myofilament Activation ◽  
Charge Movements

The effects of tetracaine on charge movements and on antipyrylazo III signals monitoring intracellular delta [Ca2+] were compared in cut frog semitendinosus muscle fibers in a single vaseline gap-voltage clamp. Low tetracaine concentrations (25-40 microM) markedly reduced delta [Ca2+] signals and shifted the rheobase. However, they neither influenced charge movement nor that peak delta [Ca2+] value associated with the contractile threshold. Higher tetracaine concentrations (100-200 microM) partly inhibited charge movements in cut fibers. They separated a steeply voltage-sensitive charge, some of whose features resembled 'q gamma' reported in intact fibers, and whose movement preceded delta [Ca2+] signals at threshold. These findings: (a) directly confirm an earlier suggestion that tetracaine acts on steps in excitation-contraction coupling rather than myofilament activation; (b) show that tetracaine at low concentrations can directly interfere with sarcoplasmic reticular calcium release without modifying charge movement; (c) show that the tetracaine-sensitive charge, first found in intact fibers, also exists in cut fibers; and (d) make it unlikely that tetracaine-sensitive charge transfer is a consequence of Ca2+ release as suggested on earlier occasions.

scholarly journals Model of Sarcomeric Ca2+ Movements, Including ATP Ca2+ Binding and Diffusion, during Activation of Frog Skeletal Muscle

1998 ◽  
Vol 112 (3) ◽  
pp. 297-316 ◽  
Author(s):  
S.M. Baylor ◽  
S. Hollingworth
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Metal Binding ◽  
Time Course ◽  
Current Knowledge ◽  
Diffusion Constant ◽  
Compartment Model ◽  
Half Width ◽  
Frog Skeletal Muscle ◽  
And Diffusion

Cannell and Allen (1984. Biophys. J. 45:913–925) introduced the use of a multi-compartment model to estimate the time course of spread of calcium ions (Ca2+) within a half sarcomere of a frog skeletal muscle fiber activated by an action potential. Under the assumption that the sites of sarcoplasmic reticulum (SR) Ca2+ release are located radially around each myofibril at the Z line, their model calculated the spread of released Ca2+ both along and into the half sarcomere. During diffusion, Ca2+ was assumed to react with metal-binding sites on parvalbumin (a diffusible Ca2+- and Mg2+-binding protein) as well as with fixed sites on troponin. We have developed a similar model, but with several modifications that reflect current knowledge of the myoplasmic environment and SR Ca2+ release. We use a myoplasmic diffusion constant for free Ca2+ that is twofold smaller and an SR Ca2+ release function in response to an action potential that is threefold briefer than used previously. Additionally, our model includes the effects of Ca2+ and Mg2+ binding by adenosine 5′-triphosphate (ATP) and the diffusion of Ca2+-bound ATP (CaATP). Under the assumption that the total myoplasmic concentration of ATP is 8 mM and that the amplitude of SR Ca2+ release is sufficient to drive the peak change in free [Ca2+] (Δ[Ca2+]) to 18 μM (the approximate spatially averaged value that is observed experimentally), our model calculates that (a) the spatially averaged peak increase in [CaATP] is 64 μM; (b) the peak saturation of troponin with Ca2+ is high along the entire thin filament; and (c) the half-width of Δ[Ca2+] is consistent with that observed experimentally. Without ATP, the calculated half-width of spatially averaged Δ[Ca2+] is abnormally brief, and troponin saturation away from the release sites is markedly reduced. We conclude that Ca2+ binding by ATP and diffusion of CaATP make important contributions to the determination of the amplitude and the time course of Δ[Ca2+].

A comparison of the effects of cationic, anionic, and neutral amphipathic agents on the contractile behaviour of frog skeletal muscle. I. Twitches and potential threshold for contraction

1984 ◽  
Vol 62 (12) ◽  
pp. 1348-1355
Author(s):  
James G. Foulks ◽  
Lillian Morishita
Keyword(s):  
Skeletal Muscle ◽  
Hydrophobic Interactions ◽  
Contractile Function ◽  
Divalent Cations ◽  
Frog Skeletal Muscle ◽  
Twitch Potentiation ◽  
Low Concentrations ◽  
Small N ◽  
Potential Threshold ◽  
Caffeine Contractures

Cationic, anionic, and neutral amphipathic agents displayed striking differences as well as similarities in their effects on the contractile function of frog skeletal muscle. Slowed repolarization during the action potential appeared to account for twitch potentiation by low concentrations of alkyl trimethylammonium and by small n-alkanols (propanol, butanol). Small n-alkanols also caused a decrease in the potential threshold for K contractures and slower relaxation of submaximum K contractures as well as enhancement of chloride withdrawal and caffeine contractures, but these effects were not observed with larger alkanols. For the ionic amphipathic agents, the direction of the changes in the relation between K0 and K-contracture tension could be accounted for on the basis of the expected changes in surface charge, but the effects of these two types of agents on the rate of relaxation of submaximum K contractures were disproportionate and with the cationic series were opposite in direction to those produced by inorganic divalent cations. The reductions in the amplitude of chloride-withdrawal contractures by cationic as well as anionic amphipaths indicated that both types of agents can impair excitation–contraction coupling. Similar depressant effects on caffeine contractures demonstrate that these responses also can be influenced by events restricted to the external lamina of the sarcolemma. It is concluded that opposite effects can be produced by similar perturbations in different regions of the sarcolemma and that electrostatic as well as hydrophobic interactions can make an important contribution to the effects of amphipathic agents on twitches and contractures in skeletal muscle.

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