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.

Effects of antipsychotic drugs on action potential production in skeletal muscle. I. Chlorpromazine and promethazine

1977 ◽  
Vol 55 (3) ◽  
pp. 452-461 ◽  
Author(s):  
H. S. Buttar ◽  
G. B. Frank
Keyword(s):  
Action Potential ◽  
Muscle Fibers ◽  
Potassium Conductance ◽  
Input Resistance ◽  
Threshold Current ◽  
Resting Potential ◽  
Sartorius Muscle ◽  
Potential Production ◽  
Drug Concentrations ◽  
Local Anaesthetic Effect

The effects of chlorpromazine, an antipsychotic phenothiazine, and promethazine, an antihistaminic phenothiazine, on excitability and action potential production in frog's sartorius muscle fibers were studied and compared. Both drugs produced a local anaesthetic effect which developed slowly over 3 to 5 h with lower concentrations (1 to 15 × 10−6 M) and was only partially reversed by exposing the muscles to a drug-free solution for 3 to 4 h. The resting potential and the input resistance of the muscle fibers were unaffected by drug concentrations which reduced the action potential maximum rate of rise, the threshold current of 2-ms injected pulses and the intracellularly measured threshold depolarization. The effects on the action potential were antagonized in an apparently competitive manner by sodium ions. Thus both drugs depressed excitability and the rising phase of the action potential by inhibiting the specific increase in sodium conductance (gNa) which normally follows an adequate stimulus. It was shown that both drugs also inhibited the secondary rise in potassium conductance (gK) which normally occurs during an action potential. Although quantitatively similar, lower concentrations of chlorpromazine (> 15 × 10−6 M) were more potent and higher concentrations (> 15 × 10−6 M) were less potent than promethazine. The qualitatively identical and the quantitatively similar effects of these two drugs would suggest that the antipsychotic effect produced by some of the phenothiazines is unrelated to their effects on action potential production.

scholarly journals Action Potential-Evoked Calcium Release Is Impaired in Single Skeletal Muscle Fibers from Heart Failure Patients

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109309 ◽  
Author(s):  
Marino DiFranco ◽  
Marbella Quiñonez ◽  
Perry Shieh ◽  
Gregg C. Fonarow ◽  
Daniel Cruz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Action Potential ◽  
Calcium Release ◽  
Muscle Fibers ◽  
Heart Failure Patients ◽  
Skeletal Muscle Fibers

scholarly journals Optical recording of action potential initiation and propagation in mouse skeletal muscle fibers

2018 ◽  
Author(s):  
Q. Banks ◽  
S.J.P. Pratt ◽  
S.R. Iyer ◽  
R.M. Lovering ◽  
E.O. Hernández-Ochoa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Conduction Velocity ◽  
Muscle Fibers ◽  
Extracellular Potassium ◽  
Bipolar Electrode ◽  
Muscle Action ◽  
Action Potential Propagation ◽  
Skeletal Muscle Fibers ◽  
Muscle Action Potential

ABSTRACTIndividual skeletal muscle fibers have been used to examine a wide variety of cellular functions and pathologies. Among other parameters, skeletal muscle action potential propagation has been measured to assess the integrity and function of skeletal muscle. In this paper, we utilize Di-8-ANEPPS, a potentiometric dye and mag-fluo-4, a low-affinity intracellular calcium indicator to non-invasively and reliably measure action potential conduction velocity in skeletal muscle. We used an extracellular bipolar electrode to generate an electric field that will initiate an action potential at one end of the fiber or the other. Using enzymatically dissociated flexor digitorum brevis (FDB) fibers, we demonstrate the strength and applicability of this technique. Using high-speed line scans, we estimate the conduction velocity to be approximately 0.4 m/s. In addition to measuring the conduction velocity, we can also measure the passive electrotonic potentials elicited by pulses by either applying tetrodotoxin (TTX) or reducing the bath sodium levels. We applied these methodologies to FDB fibers under elevated extracellular potassium conditions, and found that the conduction velocity is significantly reduced compared to our control concentration. Lastly, we have constructed a circuit model of a skeletal muscle in order to predict passive polarization of the fiber by the field stimuli. Our predictions from the model fiber closely resemble the recordings acquired from in vitro assays. With these techniques, we can examine how many different pathologies and mutations affect skeletal muscle action potential propagation. Our work demonstrates the utility of using Di-8-ANEPPS or mag-fluo-4 to non-invasively measure action potential conduction velocity.

scholarly journals Optical Recording of Action Potential Initiation and Propagation in Mouse Skeletal Muscle Fibers

2018 ◽  
Vol 115 (11) ◽  
pp. 2127-2140
Author(s):  
Quinton Banks ◽  
Stephen Joseph Paul Pratt ◽  
Shama Rajan Iyer ◽  
Richard Michael Lovering ◽  
Erick Omar Hernández-Ochoa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Fibers ◽  
Optical Recording ◽  
Mouse Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Initiation And Propagation ◽  
Action Potential Initiation ◽  
Potential Initiation

The Collapse of the Sarcoplasmic Reticulum in Skeletal Muscle

1978 ◽  
Vol 33 (7-8) ◽  
pp. 561-573 ◽  
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace ◽  
Wilhelm Hasselbach
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Fibers ◽  
Membrane Capacitance ◽  
Frog Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Plausible Mechanism

Abstract When various cations, including Ca2+, are in the fixative, both sarcoplasmic reticulum (SR) of whole skeletal muscle and isolated SR vesicles collapse to form pentalaminate “compound membranes” that result from the apparent fusion of the lumenal lamellae of the membranous envelope of the SR. The process may be reversed by subsequently soaking the tissue in 1 ᴍ NaCl. An identical morphological phenomenon is observed in unfixed quickly frozen isolated frog skeletal muscle fibers, the cation in that case coming from endogenous sources. The hypothesis is advanced that the collapse is an in vivo process mediated by the sequestration of Ca2+ after contraction. The resulting obliteration of the SR lumen would have the effect of displacing the SR contents into the junctional SR, as well as electrically isolating the free SR from the junctional SR during relaxation. As a consequence, resistive coupling between the plasmalemma and the junctional SR becomes a plausible mechanism for the translation of the action potential into Ca2+ release, since the bulk of the SR membrane capacitance would now remain separated from the plasmalemma during relaxation.

Effects of antipsychotic drugs on action potential production in skeletal muscle. II. Haloperidol: nonspecific and opiate drug receptor mediated effects

1977 ◽  
Vol 55 (3) ◽  
pp. 462-470 ◽  
Author(s):  
H. D. Durham ◽  
G. B. Frank ◽  
J. Marwaha
Keyword(s):  
Action Potential ◽  
Potassium Conductance ◽  
Sartorius Muscle ◽  
Potential Production ◽  
Mediated Effects ◽  
Low Concentrations ◽  
Adequate Stimulus ◽  
Intracellular Microelectrodes ◽  
Drug Receptor ◽  
Opiate Drug

The effects of haloperidol, an antipsychotic butyrophenone, on excitability and action potential production in frog's sartorius muscle fibers were studied. This drug produced a local-anaestheticlike effect which developed slowly over 1 to 5 h with lower concentrations (2.7 to 5.3 × 10−6 M) but was completely reversed by exposing the muscles to a drug-free solution. In studies with intracellular microelectrodes, evidence was obtained showing that haloperidol decreased excitability and depressed action potential production by inhibiting the specific increase in sodium conductance (gNa) which normally follows an adequate stimulus. Evidence also was obtained showing an inhibition of the secondary increase in potassium conductance (gK). Haloperidol is structurally related to meperidine and it was found that the inhibition of gNa produced by haloperidol is partially antagonized by low concentrations of naloxone (2.8 × 10−8 and 2.8 × 10−7 M); as was previously shown for meperidine. Thus haloperidol, like meperidine, suppresses action potential production by two mechanisms of action: one, a nonspecific local-anaestheticlike effect; and the other, a specific inhibition of gNa mediated by means of an opiate drug receptor associated with the muscle fiber membrane. Naloxone did not antagonize the effects of chlorpromazine on gNa.

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.

Voltage sensor movements of CaV1.1 during an action potential in skeletal muscle fibers

2021 ◽  
Vol 118 (40) ◽  
pp. e2026116118
Author(s):  
Quinton Banks ◽  
Hugo Bibollet ◽  
Minerva Contreras ◽  
Daniel F. Bennett ◽  
Roger A. Bannister ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Fibers ◽  
Voltage Sensor ◽  
Fluorescence Signal ◽  
Charge Movement ◽  
Electrical Measurements ◽  
Voltage Sensing ◽  
Skeletal Muscle Fibers

The skeletal muscle L-type Ca2+ channel (CaV1.1) works primarily as a voltage sensor for skeletal muscle action potential (AP)-evoked Ca2+ release. CaV1.1 contains four distinct voltage-sensing domains (VSDs), yet the contribution of each VSD to AP-evoked Ca2+ release remains unknown. To investigate the role of VSDs in excitation–contraction coupling (ECC), we encoded cysteine substitutions on each S4 voltage-sensing segment of CaV1.1, expressed each construct via in vivo gene transfer electroporation, and used in cellulo AP fluorometry to track the movement of each CaV1.1 VSD in skeletal muscle fibers. We first provide electrical measurements of CaV1.1 voltage sensor charge movement in response to an AP waveform. Then we characterize the fluorescently labeled channels’ VSD fluorescence signal responses to an AP and compare them with the waveforms of the electrically measured charge movement, the optically measured free myoplasmic Ca2+, and the calculated rate of Ca2+ release from the sarcoplasmic reticulum for an AP, the physiological signal for skeletal muscle fiber activation. A considerable fraction of the fluorescence signal for each VSD occurred after the time of peak Ca2+ release, and even more occurred after the earlier peak of electrically measured charge movement during an AP, and thus could not directly reflect activation of Ca2+ release or charge movement, respectively. However, a sizable fraction of the fluorometric signals for VSDs I, II, and IV, but not VSDIII, overlap the rising phase of charge moved, and even more for Ca2+ release, and thus could be involved in voltage sensor rearrangements or Ca2+ release activation.

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