TETRAETHYLAMMONIUM-INDUCED CONTRACTIONS OF FROG'S SKELETAL MUSCLE: I. GENERAL CONSIDERATIONS

1967 ◽  
Vol 45 (5) ◽  
pp. 821-831 ◽  
Author(s):  
G. Beaulieu ◽  
G. B. Frank
Keyword(s):  
Latent Period ◽  
Neuromuscular Transmission ◽  
Nerve Endings ◽  
Induced Response ◽  
Sartorius Muscle ◽  
Muscle Twitching ◽  
Release Of Acetylcholine ◽  
Intramuscular Nerve ◽  
Unmyelinated Nerve ◽  
Indirect Stimulation

The mechanism for the production of the 'twitching' response induced by tetraethylammonium (TEA) of the frog's sartorius muscle was investigated. A linear relation was found between the log TEA concentration and the log of the latent period for the onset of the muscle response. The minimum latent period was 5 to 10 sec. Previously it was suggested that TEA caused the release of acetylcholine from intramuscular nerve endings to produce this response (13). The findings that blocking neuromuscular transmission by d-tubocurarine, by reduced extracellular calcium concentrations, or by repetitive indirect stimulation in the presence of hemicholinium also prevented the TEA-induced muscle 'twitching' response support the above suggestion. Exposing the preparation to procaine concentrations too low to block neuromuscular transmission blocked the TEA-induced response, indicating that this response was due to an effect of TEA on the unmyelinated nerve endings.

TETRAETHYLAMMONIUM-INDUCED CONTRACTIONS OF FROG'S SKELETAL MUSCLE: III. MECHANISM OF ACTION BY CALCIUM RELEASE

1967 ◽  
Vol 45 (5) ◽  
pp. 845-855 ◽  
Author(s):  
G. Beaulieu ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Mechanism Of Action ◽  
Binding Sites ◽  
Neuromuscular Transmission ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Sartorius Muscle ◽  
Free Solution ◽  
Muscle Twitching ◽  
Solution Bathing

The effects of changes in the extracellular calcium concentration on the muscle 'twitching' response induced by tetraethylammonium of the frog's sartorius muscle were investigated. Decreasing the calcium concentration of a solution bathing the muscle increased the sensitivity of the muscle to TEA stimulation. However, with a sufficient calcium reduction (to 0.108 mM in most preparations) the muscles became completely insensitive to TEA stimulation. In contrast, calcium reduction resulted only in an increased muscle sensitivity to carbachol stimulation. Increasing the calcium concentration greatly decreased TEA sensitivity, and at 2.16 mM calcium a TEA-induced muscle 'twitching' response no longer could be produced. At this calcium concentration carbachol sensitivity was reduced but not eliminated and neuromuscular transmission was essentially unmodified. In studies with the toe muscle, it was found that TEA could restore the potassium-induced contracture that had been eliminated by soaking the muscle in a calcium-free solution. This effect of TEA was dependent upon the presence of a store of bound calcium in the muscle. These results are consistent with the hypothesis that TEA acts by releasing calcium from binding sites on the nerve endings, leading to an increased excitability and instability of these structures and resulting in the muscle twitching response. Other effects of TEA similar to those of increases in calcium are due to an increased level of ionized calcium at nerve and muscle membranes which also results from the release by TEA of calcium from membrane sites.

Dantrolene Sodium: Effects on Crustacean Muscle

1974 ◽  
Vol 52 (4) ◽  
pp. 887-890 ◽  
Author(s):  
L. L. Odette ◽  
H. L. Atwood
Keyword(s):  
Skeletal Muscle ◽  
Electrical Properties ◽  
Neuromuscular Transmission ◽  
Contractile Response ◽  
Callinectes Sapidus ◽  
Muscle Membrane ◽  
Dantrolene Sodium ◽  
Muscle Contractile ◽  
Indirect Stimulation ◽  
Vertebrate Skeletal Muscle

The effect of dantrolene sodium, a muscle relaxant effective on vertebrate skeletal muscle, has been studied on the stretcher muscle of a crab (Callinectes sapidus). The drug rapidly and reversibly attenuates the muscle contractile response to direct and indirect stimulation. Neuromuscular transmission is unaffected, as are the electrical properties of the muscle membrane. It is concluded that dantrolene sodium uncouples excitation–contraction mechanisms in crustacean tonic muscle.

Some Observations on the Physiology and Pharmacology of the Nerve Endings in the Crop and Gizzard of the Earthworm, with Special Reference to the Effects of Cooling

1945 ◽  
Vol 21 (1-2) ◽  
pp. 46-57
Author(s):  
N. AMBACHE ◽  
A. ST J. DIXON ◽  
E. A. WRIGHT
Keyword(s):  
Ganglion Cells ◽  
Rhythmic Activity ◽  
Inhibitory Effect ◽  
Nerve Endings ◽  
Rhythmic Movements ◽  
Cholinergic Nerve ◽  
Enteric Plexus ◽  
Small Doses ◽  
Release Of Acetylcholine ◽  
Parasympathetic Ganglion

1. The effect of cooling on the properties of the crop and gizzard of the earthworm has been investigated. Evidence is advanced that the rhythmic movements of the ‘warm’ preparation are neurogenic in origin and peristaltic in nature. They are abolished by nicotine and by cooling, but not by atropine. 2. Acetylcholine contracts the muscle in the crop and gizzard. This effect is abolished by atropine. The excitability of the muscle to acetylcholine is not lost after cooling. 3. Peristalsis is accompanied in the ‘warm’ preparation by a continual liberation of acetylcholine. This is absent in cold preparations. The disappearance of rhythmic activity in these is associated with the loss of acetylcholine synthesis. 4. In the ‘warm’ crop and gizzard, potassium produces contraction which is enhanced by eserine, but not abolished by nicotine or by atropine. With higher doses of potassium, stimulation is followed by inhibition. After short periods of cooling, the motor response to potassium is lost, but the inhibitory effect is still present. Prolonged cooling abolishes both actions. It is suggested that the augmentor action of potassium is due to an intermediate release of acetylcholine from the cholinergic nerve endings, and the inhibitory action to a liberation of adrenaline from the adrenergic nerves in the crop and gizzard. 5. Calcium inhibits the rhythmic activity of ‘warm’ preparations, and the effect of potassium. It has no action on cooled preparations, and in these it does not affect the contractions produced by acetylcholine. It is suggested that calcium acts on ‘warm’ preparations by preventing the release of acetylcholine from cholinergic nerve endings. 6. The action of adrenaline on ‘warm’ preparations is twofold: small doses have an augmentor effect; larger doses are inhibitory. After cooling, adrenaline has no action by itself. It is suggested that the augmentor effect of adrenaline is due to an improvement in acetylcholine-transmission at the cholinergic nerve endings. 7. Small doses of barium contract the ‘warm’ preparation. This action is inhibited by calcium, abolished by nicotine, and is lost after cooling. It is suggested that the action of such doses of barium is due to a stimulation of parasympathetic ganglion cells. 8. The presence of multipolar nerve cells in the enteric plexus was demonstrated in histological sections of the crop and gizzard. These were found lying between the circular and longitudinal muscle layers, in a position analogous to that of Auerbach's plexus.

Effect of Cooling on Neuromuscular Transmission in the Frog

1958 ◽  
Vol 192 (3) ◽  
pp. 464-470 ◽  
Author(s):  
Choh-Luh Li ◽  
Peter Gouras
Keyword(s):  
Critical Temperature ◽  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
Neuromuscular Transmission ◽  
The Other ◽  
Sartorius Muscle ◽  
Single Muscle ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials ◽  
Muscle Responses

Recording with intracellular electrodes from endplate regions of frogs sartorius muscle showed that at –1°C miniature endplate potentials still occurred and that the resting membrane potentials differed very little from those recorded at room temperatures. The miniature potentials, however, were decreased in frequency and increased in amplitude by cooling; and at about 5°C, the amplitude began to fall while the frequency continued to be low. It was also at about 5°C that the muscle responses to nerve stimulation frequently consisted of endplate potentials only. Upon rewarming spike potentials again appeared. These observations suggest that there is a critical temperature for neuromuscular transmission, below which impediment of impulse transmission began; and in the frog it is 5°C. The experiments also demonstrated that during the process of cooling a blockage of impulses at one neuromuscular junction and transmission across the other in a single muscle fiber could occur.

Neuromuscular transmission in dystrophic mice

1977 ◽  
Vol 40 (4) ◽  
pp. 836-843 ◽  
Author(s):  
S. Carbonetto
Keyword(s):  
Neuromuscular Transmission ◽  
Neuromuscular Junctions ◽  
Large Population ◽  
Muscle Fibers ◽  
Dystrophic Muscle ◽  
Quantum Content ◽  
Quantal Size ◽  
Significant Difference ◽  
Release Of Acetylcholine ◽  
Dystrophic Mice

1. Neuromuscular transmission was studied in the extensor digitorum-longus muscle of dystrophic mice (strain 129/ReJ) by means of intracellular recording techniques. 2. In a large population of normal and dystrophic muscle fibers tested, the incidence of transmission failure was about 2% and showed no significant difference between the two groups. 3. Quantal size and quantum content of dystrophic junctions were found to be normal. This was true even of nerve terminal on apparently atrophied muscle fibers. 4. The facilitation ratio at dystrophic junctions was not significantly different from normal. 5. Dystrophic neuromuscular junctions exhibited an abnormality high frequency of giant spontaneous potentials. Application of tetrodotoxin (10(-6) M) and curare (10(-6) M) indicated that these potentials were caused by impulse-independent release of acetylcholine. 6. Neuromuscular transmission in dystrophic mice was found functionally normal and unrelated to the degenerative state of the muscle.

THE INTRAMUSCULAR NERVE ENDINGS IN MYASTHENIA GRAVIS

Brain ◽  
1960 ◽  
Vol 83 (1) ◽  
pp. 10-23 ◽  
Author(s):  
E. R. BICKERSTAFF ◽  
A. L. WOOLF
Keyword(s):  
Myasthenia Gravis ◽  
Nerve Endings ◽  
Intramuscular Nerve

Intramuscular nerve fibres in disorders of neuromuscular transmission

1986 ◽  
Vol 88 (1) ◽  
pp. 71
Author(s):  
F.G.I. Jennekens ◽  
L.M.E. Smit ◽  
C.J.M. v.d. Oord ◽  
H. Veldman ◽  
B.S. Oen ◽  
...  
Keyword(s):  
Neuromuscular Transmission ◽  
Nerve Fibres ◽  
Intramuscular Nerve
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