The Effects of Pentobarbital on the Electrical and Mechanical Properties of Frog and Snake Twitch Muscle Fibers

1973 ◽  
Vol 51 (2) ◽  
pp. 68-78 ◽  
Author(s):  
J. G. Foulks ◽  
Florence A. Perry ◽  
H. D. Sanders ◽  
H. Washio

Pentobarbital (0.4–1.2 mM) produces marked enhancement of twitch tension in frog skeletal muscle. Latency is reduced and the rate of tension development is increased. In ordinary media, the agent impairs K contractures but this depressant effect can be eliminated by using a high calcium medium containing acetate in place of chloride. In such solutions, pentobarbital reduces the [K]0 necessary for K contractures. In snake twitch fibers depolarized by means of a voltage clamp, pentobarbital shifted the relation between membrane potential and contracture tension to a more negative level of potential. High concentrations of pentobarbital have a depolarizing effect which is greatly accentuated in a medium containing no permeant anion. The drug reduces the rate and extent of the depolarization produced by elevation of [K]0, and increases membrane resistance. These observations indicate that pentobarbital reduces the potassium permeability of the surface membrane of twitch muscle fibers.

1973 ◽  
Vol 61 (2) ◽  
pp. 176-184 ◽  
Author(s):  
Hiroshi Washio

The effect of glycerol treatment on the membrane currents and tension development was studied in voltage clamped snake muscle fibers. In muscle fibers which were exposed for 1 h to a normal saline containing 400 mM glycerol and then returned to a normal medium, graded depolarizations did not accompany contractile responses. However, when the fiber was depolarized to a certain level, an increment of outward current appeared which partially inactivated with time. The threshold for delayed rectification in glycerol-treated fibers was almost the same as that of intact fibers in spite of the absence of contractile tension. The results suggest that the delayed rectification may be attributed at least in part to the surface membrane and that the contractile activation probably does not depend simply on the inactivating outward currents through the delayed rectification channel.


1966 ◽  
Vol 49 (5) ◽  
pp. 963-976 ◽  
Author(s):  
Arthur A. Manthey

Desensitization, as represented by the progressive decline in the electromotive effects of depolarizing agents at the neuromuscular junction, was studied by observing the time course of changes in effective transmembrane resistance during the prolonged application of 0.27 mM carbamylcholine to the postjunctional region of frog skeletal muscle fibers. The effective transmembrane resistance was measured by means of two intracellular microelectrodes implanted in the junctional region of single muscle fibers. When carbamylcholine was applied to the muscle there was an immediate decrease in the effective membrane resistance followed by a slower return toward control values which was identified as the phase of desensitization. When the calcium concentration was increased from 0 to 10 mM there was an approximately sevenfold increase in the rate of desensitization. On the other hand, an increase in the concentration of sodium from 28 to 120 mM caused a slowing of the rate of desensitization. Even in muscles depolarized by potassium sulfate, calcium increased the rate of desensitization while high concentrations of potassium tended to prolong the process. Some mechanisms by which calcium might exert these effects are discussed.


1972 ◽  
Vol 50 (1) ◽  
pp. 37-44 ◽  
Author(s):  
E. C. Vos ◽  
G. B. Frank

A brief exposure (about 10–30 s) of a frog's toe muscle or a small bundle of fibers from the semi-tendinosus muscle to just subthreshold potassium concentrations potentiated contractures subsequently produced by exposing the muscles to a potassium concentration slightly above the threshold. The contractures thus potentiated had greater maximum tensions, and greater rates of tension development and relaxation than control contractures elicited by the same final potassium concentration. The resistance to stretch (R.T.S.) in the first few seconds of the potentiated contractures was about twice that of control contractures. Maximum potentiation occurred with preexposures of about 30 s; longer preexposures led to a decrease of potentiation and eventually to a depression of the contracture. The potentiation was not immediately abolished when the muscle was reexposed to Ringer solution but persisted for 2 min or longer (the 'washout effect'). It was concluded that exposing a muscle to low subcontracture threshold concentrations of potassium for a few seconds primes the intracellular contractile apparatus, probably by causing an increased sarcoplasmic concentration of Ca2+ ions, resulting in a potentiation of subsequently induced submaximal potassium contractures. The increase in metabolism (or 'Solandt effect') seen under these conditions is temporally related to the decline and eventual loss of the potentiation and is probably a reflection of active processes involved in reducing the sarcoplasmic concentration of Ca2+ ions.


Toxicon ◽  
1987 ◽  
Vol 25 (2) ◽  
pp. 159-165 ◽  
Author(s):  
S.L. Hu ◽  
C.Y. Kao ◽  
F.E. Koehn ◽  
H.K. Schnoes

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank

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.


1995 ◽  
Vol 37 (5) ◽  
pp. 637-645 ◽  
Author(s):  
Marcello Villanova ◽  
Jean Pierre Louboutin ◽  
Danielle Chateau ◽  
Bruno Eymard ◽  
Marguerite Sagniez ◽  
...  

1977 ◽  
Vol 55 (5) ◽  
pp. 1122-1134 ◽  
Author(s):  
J. G. Foulks ◽  
Florence A. Perry ◽  
P. Tsang

The depressant effect of acidity on twitches and K contractures in frog skeletal muscle was greatly accentuated in the presence of organic anions, particularly anions such as butyrate, which also reduced these responses at neutral pH. Conversely, alkaline pH antagonized the depression of contractile responses by butyrate. Most of the effects of acid pH were rapid in onset and were accomplished without any change in membrane resting or action potentials, although depolarization developed in the presence of carboxylate anions when pH was reduced below 6.0. Simultaneous variation in pH and butyrate concentration showed that the undissociated acid exerted a prominent depressant effect only when its concentration reached 1–10 mM, and that the marked depressant action of butyrate at neutral pH was produced primarily by the dissociated anion. Similar experiments showed that the dissociated anion also was largely responsible for the enhanced depolarizing effect of acidity in media containing carboxylates. Acid-induced depolarization was not facilitated in media containing methane sulfonate, but in spite of its low pKa, this anion also increased the sensitivity of contractile responses to the depressant effects of acidity. Hence, the accentuation of the effects of organic anions by acid pH must be exerted on the sequence of membrane events which link excitation and contraction. The effect of acidity was greater when longer apolar hydrocarbon chains were attached to the anionic group for both the carboxylate and the sulfonate series of ions. These depressant effects may be produced by interference with the membrane-stabilizing actions of divalent cations, and may involve increased membrane fluidity.


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