scholarly journals ERRATUM: Everett A.W. 1999. Membrane Recycling Due to Low and High Rates of Nerve Stimulation at Release Sites in the Amphibian (Bufo marinus) Neuromuscular Junction. Synapse 32:110-118.

Synapse ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 81-81
Author(s):  
A.W. Everett
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
Bufo Marinus ◽  
Membrane Recycling

Repetitive Nerve Stimulation Studies

2016 ◽  
pp. 328-346
Author(s):  
Kathleen D. Kennelly
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
Nerve Conduction ◽  
Neuromuscular Transmission ◽  
Repetitive Stimulation ◽  
Nerve Conduction Studies ◽  
Clinical Correlation ◽  
Repetitive Nerve Stimulation ◽  
Anatomy And Physiology

Repetitive stimulation is a technique that evaluates the function of the neuromuscular junction. It is important not only in the detection, clarification, and follow-up of neuromuscular junction diseases, but also in excluding these disorders in patients with symptoms of fatigue, vague weakness, diplopia, ptosis, and malaise, or with objective weakness of uncertain origin. The technique requires knowledge of the physiology and pathophysiology of neuromuscular transmission and the basic techniques of nerve conduction studies. This chapter includes a brief review of the anatomy and physiology of the neuromuscular junction as it applies to repetitive stimulation, a detailed discussion of the technique, the pitfalls that can occur if not carried out correctly, criteria used to classify the results as normal or abnormal, the patterns of abnormalities that can be seen, and the clinical correlation of those abnormalities with the various different disorders of neuromuscular transmission.

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.

Case 24

2018 ◽  
Author(s):  
Bashar Katirji
Keyword(s):  
Botulinum Toxin ◽  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
Clostridium Botulinum ◽  
Anaerobic Bacteria ◽  
Neuromuscular Disorder ◽  
Repetitive Nerve Stimulation ◽  
Myasthenic Syndrome ◽  
High Index Of Suspicion ◽  
Foodborne Botulism

Botulism is an extremely rare neuromuscular disorder, caused by botulinum toxin which is produced by the anaerobic bacteria Clostridium botulinum. It has several forms: classic foodborne, infantile, wound, intestinal, and iatrogenic forms. The presentation is often acute and severe but may be occasionally subacute and moderate. The diagnosis may be difficult and requires a high index of suspicion. This case presents an adult with classic foodborne botulism and highlights the clinical and electrodiagnostic findings that distinguish this disorder from other neuromuscular junction disorders including myasthenia gravis and Lambert-Eaton myasthenic syndrome. Specifically, the findings on repetitive nerve stimulation are discussed and distinguished from the results seen in other neuromuscular junction disorders.

Pathophysiological associations in paediatric neuromuscular junction disorders

2017 ◽  
Author(s):  
Matthew Pitt
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Compound Muscle Action Potential ◽  
Paediatric Population ◽  
Neuromuscular Blocking ◽  
Repetitive Nerve Stimulation ◽  
Long Duration ◽  
Muscle Action Potential ◽  
Autoimmune Conditions

Myasthenia can be caused by acquired or autoimmune conditions and other conditions resulting from genetic abnormalities of the proteins in the neuromuscular junction. The clinical clues to diagnosis in the paediatric population are highlighted in this chapter. Among these are sudden death, episodic apnoea, stridor, association with myopathy, and limb-girdle weakness presentation. Acquired disorders of the neuromuscular junction occur, such as infantile botulism, tick paralysis, and persistence of neuromuscular blocking agents. Some patterns of abnormality are seen in the neurophysiological findings, the most notable of which is a repetitive compound muscle action potential at low rates of stimulation. Decrement only seen after long-duration, high-frequency repetitive nerve stimulation is described in choline acetyltransferase (CHAT) abnormalities. DOK7 myasthenia may demonstrate patchy abnormalities of jitter and this is described along with the profound increment of the high-frequency repetitive nerve stimulation in Lambert–Eaton syndrome.

scholarly journals THE LOCALIZATION OF ACETYLCHOLINESTERASE AT THE AUTONOMIC NEUROMUSCULAR JUNCTION

1967 ◽  
Vol 33 (1) ◽  
pp. 93-102 ◽  
Author(s):  
Peter M. Robinson ◽  
Christopher Bell
Keyword(s):  
Enzyme Activity ◽  
Smooth Muscle ◽  
Neuromuscular Junction ◽  
Smooth Muscle Cells ◽  
Schwann Cells ◽  
Synaptic Vesicles ◽  
Muscle Cells ◽  
Acetylcholinesterase Activity ◽  
Bufo Marinus ◽  
Toad Bufo

Acetylcholinesterase has been localized at the autonomic neuromuscular junction in the bladder of the toad (Bufo marinus) by the Karnovsky method. High levels of enzyme activity have been demonstrated in association with the membranes of cholinergic axons and the adjacent membranes of the accompanying Schwann cells. The synaptic vesicles stained in occasional cholinergic axons. After longer incubation times, the membrane of smooth muscle cells close to cholinergic axons also stained. Axons with only moderate acetylcholinesterase activity or with no activity at all were seen in the same bundles as cholinergic axons, but identification of the transmitter in these axons was not possible.

Kinetics of acetylcholine quanta release at the neuromuscular junction during high-frequency nerve stimulation

2010 ◽  
Vol 32 (9) ◽  
pp. 1480-1489 ◽  
Author(s):  
Irina V. Kovyazina ◽  
Andrei N. Tsentsevitsky ◽  
Evgeny E. Nikolsky ◽  
Ellya A. Bukharaeva
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Kinetics Of

Delayed Synaptic Transmission in Drosophila cacophonynull Embryos

2008 ◽  
Vol 100 (5) ◽  
pp. 2833-2842 ◽  
Author(s):  
Jiamei Hou ◽  
Takuya Tamura ◽  
Yoshiaki Kidokoro
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Nerve Stimulation ◽  
Wild Type ◽  
Synaptic Currents ◽  
Voltage Gated ◽  
Delayed Release ◽  
Spider Toxin ◽  
High K

Ca2+ influx through the Drosophila N-type Ca2+ channel, encoded by cacophony ( cac), triggers fast synaptic transmission. We now ask whether the cac Ca2+ channel is the Ca2+ channel solely dedicated for fast synaptic transmission. Because the cac null mutation is lethal, we used cac null embryos to address this question. At the neuromuscular junction in HL3 solution, no fast synchronous synaptic transmission was detected on nerve stimulation. When the wild-type cac gene was introduced in the cac null background, fast synaptic transmission recovered. However, even in cac null embryos, nerve stimulation infrequently induced delayed synaptic events in the minority of cells in 1.5 mM [Ca2+]e and in the majority of cells in 5 mM [Ca2+]e. The number of delayed quantal events per stimulus was greater in 5 mM [Ca2+]e than in 1.5 mM. Thus the delayed release is [Ca2+]e dependent. Plectreurys toxin II (PLTXII) (10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca2+ channels, other than cac Ca2+ channels, are contributing to them. However, delayed events were not affected by 50 μM La3+. The frequency of miniature synaptic currents in cac null embryos was ∼1/2 of control, whereas in high K+ solutions, it was ∼1/135. The hypertonicity response was ∼1/10 of control. These findings indicate that the number of release-ready vesicles is smaller in cac null embryos. Taken together, the cac Ca2+ channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca2+ channel, the non- cac, PLTXII-sensitive Ca2+ channel, is contributing to delayed release in cacnull embryos.

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