Has nonquantal acetylcholine secretion from motor nerve endings a role in neurotrophic control of resting membrane potential in rat muscle fibers?

1986 ◽  
Vol 17 (3) ◽  
pp. 258-264
Author(s):  
E. M. Volkov ◽  
V. N. Frosin ◽  
G. I. Poletaev
Keyword(s):  
Membrane Potential ◽  
Motor Nerve ◽  
Muscle Fibers ◽  
Nerve Endings ◽  
Resting Membrane Potential ◽  
Neurotrophic Control ◽  
Rat Muscle

Role of calcium ions and spike activity in the neurotrophic control of membrane potential in rat muscle fibers

1988 ◽  
Vol 19 (4) ◽  
pp. 329-334
Author(s):  
A. Kh. Urazaev ◽  
A. V. Chikin ◽  
E. M. Volkov ◽  
G. I. Poletaev ◽  
Kh. S. Khamitov
Keyword(s):  
Membrane Potential ◽  
Calcium Ions ◽  
Spike Activity ◽  
Muscle Fibers ◽  
Neurotrophic Control ◽  
Rat Muscle

Blockers of potassium current and resting membrane potential in rat muscle fibers

Life Sciences ◽  
1992 ◽  
Vol 51 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Adriana S. Losavio ◽  
O. Delbono ◽  
S. Muchnik ◽  
B.A. Kotsias
Keyword(s):  
Membrane Potential ◽  
Potassium Current ◽  
Muscle Fibers ◽  
Resting Membrane Potential ◽  
Rat Muscle

Effect of insulin on membrane potential and potassium content of rat muscle

1959 ◽  
Vol 197 (3) ◽  
pp. 515-523 ◽  
Author(s):  
Kenneth L. Zierler
Keyword(s):  
Membrane Potential ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Potassium Content ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Conventional Theory ◽  
Rat Muscle

Insulin increased resting membrane potential of excised rat muscle, extensor digitorum longus, by about 5 mv in less than 1 hour. In 1 hour insulin caused no increase in the ratio of intra- to extracellular potassium, but in 2–3 hours intracellular K increased by about 10%. It is concluded that the increase in intracellular K is probably too small and too late to account for the hyperpolarization on the basis of conventional theory and it is suggested that the hyperpolarization produced by insulin is the cause of the potassium shift.

TETRAETHYLAMMONIUM-INDUCED CONTRACTIONS OF FROG'S SKELETAL MUSCLE: II. EFFECTS ON INTRAMUSCULAR NERVE ENDINGS

1967 ◽  
Vol 45 (5) ◽  
pp. 833-844 ◽  
Author(s):  
G. Beaulieu ◽  
G. B. Frank ◽  
F. Inoue
Keyword(s):  
Motor Nerve ◽  
Muscle Fibers ◽  
Electrical Stimulus ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Nerve Endings ◽  
Glass Capillary ◽  
Action Potential Firing ◽  
Low Concentrations ◽  
Potential Firing

By recording simultaneously from muscle fibers and from the ventral root supplying the muscle, it was found that low concentrations of tetraethylammonium (TEA) caused the muscle fibers to fire without antidromic impulses being conducted to the ventral root. Exposing the muscles to higher TEA concentrations induced action potential firing in both the muscle and the ventral root. d-Tubocurarine prevented the muscle fiber activity but did not modify the ventral root firing. The application of a single supramaximal electrical stimulus to the sciatic nerve resulted in an afterdischarge of the muscle fibers either alone or simultaneous with an afterdischarge of fibers in the ventral root. By recording from fine intramuscular motor nerve fibers with extracellular glass capillary microelectrodes while simultaneously recording from the ventral root, it was demonstrated that TEA could cause these fine intramuscular motor nerve fibers to fire without the activity being conducted antidromically to the ventral root. A consideration of the patterns of TEA-induced electrical activity and afterdischarging led to the suggestion that TEA causes these effects by displacing calcium from binding sites on the motor nerve endings, making the latter hyperexcitable and unstable and thereby causing afterdischarging and 'spontaneous' activity.

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