Pre‐ and post‐synaptic actions of botulinum toxin at the rat neuromuscular junction.

Sellin, Lawrence C.; Thesleff, S.

doi:10.1113/jphysiol.1981.sp013838

Cited by 65 publications

(31 citation statements)

References 18 publications

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“…These m.e.p.p.s have a more variable, but generally much longer, time-to-peak than m.e.p.p.s at unpoisoned junctions, and their amplitude is frequently larger, shifting the distribution of m.e.p.p. amplitudes towards the right (Sellin & Thesleff, 1981;Colmeus, Gomez, Molgo6 & Thesleff, 1982;Thesleff, Molgo & Lundh, 1983). Fundamentally, these m.e.p.p.s differ from those at unpoisoned junctions by being unaffected in frequency by procedures which alter extra-or intracellular Ca2+ concentrations.…”

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confidence: 97%

“…It is concluded that enhancement ofslow m.e.p.p. frequency in muscles poisoned INTRODUCTION Botulinum toxin type A (BoTx) is a presynaptically acting neurotoxin with a specific and long-lasting effect at cholinergic nerve endings (for recent reviews, see Simpson, 1981;Sellin, 1981). At the neuromuscular junction its actions are characterized by a block of impulse-evoked release of acetylcholine (ACh) and by a marked reduction in the frequency of spontaneous miniature end-plate potentials (m.e.p.p.s).…”

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confidence: 99%

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Miniature end‐plate potentials in rat skeletal muscle poisoned with botulinum toxin.

Kim¹,

Lømo²,

Lupa³

et al. 1984

The Journal of Physiology

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SUMMARY1. Spontaneous transmitter release, recorded as miniature end-plate potentials (m.e.p.p.s), was studied in rat extensor digitorum longus (e.d.l.) and soleus muscles partially or completely paralysed by botulinum toxin type A (BoTx). Normal unpoisoned muscles were examined for comparison.2. Analysis of m.e.p.p.s in both normal and BoTx-poisoned muscles confirmed the presence of two populations of potentials. One population, which comprised about 96 % of the m.e.p.p.s recorded at non-poisoned end-plates, was characterized by a uniform time course and a mean time-to-peak of 0 5-0-7 ms. These potentials had a shape and time-to-peak similar to that of quantal end-plate potentials (e.p.p.s) evoked by nerve stimuli. These were designated 'fast m.e.p.p.s'. The other population of m.e.p.p.s was characterized by a slower, more variable rise-time, the time-to-peak exceeding 141 ms, and generally a larger amplitude. These were designated 'slow m.e.p.p.s'.3. In both partial and complete paralysis by BoTx the frequency of fast m.e.p.p.s was reduced by more than 90 % and the reduction lasted several weeks. After 6-10

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confidence: 97%

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confidence: 99%

Miniature end‐plate potentials in rat skeletal muscle poisoned with botulinum toxin.

Kim¹,

Lømo²,

Lupa³

et al. 1984

The Journal of Physiology

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“…The conductance was obtained from y = 12/(l.E) where 12 is the current noise variance, I the mean current passed and E the clamp potential. The reversal potential was taken as o mV (Colquhoun et al, 1977;Sellin & Thesleff, 1981;Alema et al, 1981). Corrections were made throughout to n, a and y for the effects of the low pass filters used (Colquhoun et al, 1977).…”

Section: Electrophysiological Recordingmentioning

confidence: 99%

The effect of chronic neostigmine treatment on channel properties at the rat skeletal neuromuscular junction

Gwilt

Wray

1986

British J Pharmacology

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1 We have studied the effects ofchronic neostigmine treatment on single channel properties at the rat skeletal neuromuscular junction. Rats received 0.86 mg kg -neostigmine (s.c.) daily for 9-11 days. Microelectrode recordings were then made from the extensor digitorum longus muscle. 2 The amplitude of miniature endplate potentials was significantly reduced in muscles from neostigmine-treated rats as compared with controls. 3 Acetylcholine (2-55 M) applied in the bath produced a depolarization and associated channel opening frequency (from voltage noise analysis) which were significantly reduced in neostigminetreated muscles with respect to controls. 4 The depolarization resulting from the opening of a single channel (from voltage noise analysis) and single channel open time and conductance (from current noise analysis) were not significantly changed by chronic neostigmine treatment. 5 It is concluded that chronic neostigmine treatment causes an adaptive reduction in the number of functional acetylcholine receptors at the endplate without otherwise affecting single channel properties themselves.

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“…Botulinum toxin (BTX) is a potent neurotoxin synthesized by the Gram-negative, anaerobic, spore-forming bacterium Clostridium botulinum. It blocks presynaptic release of Ach into the end plate of the neural junction, thus leading to reduced activity of muscles or glands (13). Until recently, increasing research has suggested independent actions of BTX on peripheral nociceptors by blocking release of neurotransmitters, including pain and inflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of botulinum toxin therapy in treatment of myofascial pain

et al. 2017

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The present study aimed to assess the efficacy of using botulinum toxin (BTX) in temporomandibular joint disorders, particularly pertaining to myofascial pain from masseter and temporal muscles. The study included 11 patients who were diagnosed with masseter and temporalis myofascial pain. Visual analog scale for pain and pressure algometry were conducted initially, after 1 month of conservative therapy (control group), and after 1 month of BTX type A injections (study group). Data were statistically analyzed (analysis of variance and Wilcoxon's test) to determine intergroup differences. Both conservative therapy and BTX injections showed reduction in pain scores and increase in pain threshold compared with baseline, and statistically significant differences were noted between both groups. Thus, BTX injections appear to be effective in management of chronic myofascial pain targeting masseter and temporalis muscles.

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Pre‐ and post‐synaptic actions of botulinum toxin at the rat neuromuscular junction.

Cited by 65 publications

References 18 publications

Miniature end‐plate potentials in rat skeletal muscle poisoned with botulinum toxin.

Miniature end‐plate potentials in rat skeletal muscle poisoned with botulinum toxin.

The effect of chronic neostigmine treatment on channel properties at the rat skeletal neuromuscular junction

Efficacy of botulinum toxin therapy in treatment of myofascial pain

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