Facilitation, augmentation and potentiation of transmitter release at frog neuromuscular junctions poisoned with botulinum toxin

1986 ◽  
Vol 406 (6) ◽  
pp. 636-640 ◽  
Author(s):  
M. T. Lupa ◽  
N. Tabti
Keyword(s):  
Botulinum Toxin ◽  
Transmitter Release ◽  
Neuromuscular Junctions

Evidence for calcium-dependent vesicular transmitter release insensitive to tetanus toxin and botulinum toxin type F

Neuroscience ◽  
1999 ◽  
Vol 90 (3) ◽  
pp. 893-902 ◽  
Author(s):  
A. Fassio ◽  
R. Sala ◽  
G. Bonanno ◽  
M. Marchi ◽  
M. Raiteri
Keyword(s):  
Botulinum Toxin ◽  
Tetanus Toxin ◽  
Transmitter Release ◽  
Botulinum Toxin Type ◽  
Calcium Dependent

Physiological effects of two FMRFamide-related peptides from the crayfish Procambarus clarkii

1995 ◽  
Vol 198 (1) ◽  
pp. 109-116
Author(s):  
M Skerrett ◽  
A Peaire ◽  
P Quigley ◽  
A Mercier
Keyword(s):  
Transmitter Release ◽  
Procambarus Clarkii ◽  
Neuromuscular Junctions ◽  
Input Resistance ◽  
Physiological Effects ◽  
Synaptic Current ◽  
Extensor Muscles ◽  
Neuromuscular Systems ◽  
Dose Dependent ◽  
Measurable Change

The present study examined the effects of two recently identified neuropeptides on crayfish hearts and on neuromuscular junctions of the crayfish deep abdominal extensor muscles. The two peptides, referred to as NF1 (Asn-Arg-Asn-Phe-Leu-Arg-Phe-NH2) and DF2 (Asp-Arg-Asn-Phe-Leu-Arg-Phe-NH2), increased the rate and amplitude of spontaneous cardiac contractions and increased the amplitude of excitatory junctional potentials (EJPs) in the deep extensors. Both effects were dose-dependent, but threshold and EC50 values for the cardiac effects were at least 10 times lower than for the deep extensor effects. The heart responded equally well to three sequential applications of peptide in any given preparation, but the responses of the deep extensors appeared to decline with successive peptide applications. The results support the hypothesis that these two neuropeptides act as neurohormones to modulate the cardiac and neuromuscular systems in crayfish. Quantal synaptic current recordings from the deep extensor muscles indicate that both peptides increase the number of quanta of transmitter released from synaptic terminals. Neither peptide elicited a measurable change in the size of quantal synaptic currents. NF1 caused a small increase in muscle cell input resistance, while DF2 did not alter input resistance. These data suggest that DF2 increases EJP amplitudes primarily by increasing transmitter release, while the increase elicited by NF1 appears to involve presynaptic and postsynaptic mechanisms.

scholarly journals Changes in miniature endplate potential frequency during repetitive nerve stimulation in the presence of Ca2+, Ba2+, and Sr2+ at the frog neuromuscular junction.

1981 ◽  
Vol 77 (5) ◽  
pp. 503-529 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Neuromuscular Junctions ◽  
Fourth Power ◽  
Bathing Solution ◽  
Frog Neuromuscular Junction ◽  
Repetitive Nerve Stimulation ◽  
Time Constants ◽  
Endplate Potential ◽  
Induced Changes

Miniature endplate potentials (MEPPs) were recorded from frog sartorious neuromuscular junctions under conditions of reduced quantal contents to study the effect of repetitive nerve stimulation on asynchronous (tonic) quantal transmitter release. MEPP frequency increased during repetitive stimulation and then decayed back to the control level after the conditioning trains. The decay of the increased MEPP frequency after 100-to 200-impulse conditioning trains can be described by four components that decayed exponentially with time constants of about 50 ms, 500 ms, 7 s, and 80 s. These time constants are similar to those for the decay of stimulation-induced changes in synchronous (phasic) transmitter release, as measured by endplate potential (EPP) amplitudes, corresponding, respectively, to the first and second components of facilitation, augmentation, and potentiation. The addition of small amounts of Ca2+ or Ba2+ to the Ca2+-containing bathing solution, or the replacement of Ca2+ with Sr2+, led to a greater increase in the stimulation-induced increases in MEPP frequency. The Sr-induced increase in MEPP frequency was associated with an increase in the second component of facilitation of MEPP frequency; the Ba-induced increase with an increase in augmentation. These effects of Sr2+ and Ba2+ on stimulation-induced changes in MEPP frequency are similar to the effects of these ions on stimulation-induced changes in EPP amplitude. These ionic similarities and the similar kinetics of decay suggest that stimulation induced changes in MEPP frequency and EPP amplitude have some similar underlying mechanisms. Calculations are presented which show that a fourth power residual calcium model for stimulation-induced changes in transmitter release cannot readily account for the observation that stimulation-induced changes in MEPP frequency and EPP amplitude have similar time-courses.

Structural and functional changes of frog neuromuscular junctions in high calcium solutions

1971 ◽  
Vol 178 (1053) ◽  
pp. 407-415 ◽  
Keyword(s):  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Secretory Response ◽  
Spontaneous Release ◽  
Functional Changes ◽  
High Calcium ◽  
Release Of Acetylcholine ◽  
Evoked Transmitter Release

When frog muscles are exposed for several hours to a solution of isotonic calcium chloride, the secretory response of the motor nerve terminals to imposed depolarization ultimately fails and the rate of spontaneous release of acetylcholine also declines towards zero. The failure of depolarization-evoked transmitter release is irreversible while spontaneous release reappears, though in highly abnormal fashion, when the muscle is returned to a normal ionic medium. Examination of motor end-plates, during various stages of calcium treatment, shows that there is gradual intra-axonal agglutination of synaptic vesicles which is only very incompletely reversible. This effect is presumably the consequence of gradual entry and intracellular accumulation of calcium ions. Analogous treatment with isotonic magnesium, while resulting in immediate loss of evoked transmitter release, does not lead to progressive agglutination of synaptic vesicles, nor to irreversible impairment of the secretory response of the nerve terminal. The possible relations between structural and functional changes during calcium and magnesium treatment are discussed.

scholarly journals Gambierol Potently Increases Evoked Quantal Transmitter Release and Reverses Pre- and Post-Synaptic Blockade at Vertebrate Neuromuscular Junctions

Neuroscience ◽  
2020 ◽  
Vol 439 ◽  
pp. 106-116
Author(s):  
Jordi Molgó ◽  
Sébastien Schlumberger ◽  
Makoto Sasaki ◽  
Haruhiko Fuwa ◽  
M. Carmen Louzao ◽  
...  
Keyword(s):  
Transmitter Release ◽  
Neuromuscular Junctions ◽  
Quantal Transmitter Release

scholarly journals Over 25 Years of Pediatric Botulinum Toxin Treatments: What Have We Learned from Injection Techniques, Doses, Dilutions, and Recovery of Repeated Injections?

Toxins ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 440
Author(s):  
Heli Sätilä
Keyword(s):  
Botulinum Toxin ◽  
Upper Limb ◽  
Neuromuscular Junctions ◽  
Pediatric Population ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Botulinum Toxin Type ◽  
Triceps Surae ◽  
Injection Techniques ◽  
The Impact

Botulinum toxin type A (BTXA) has been used for over 25 years in the management of pediatric lower and upper limb hypertonia, with the first reports in 1993. The most common indication is the injection of the triceps surae muscle for the correction of spastic equinus gait in children with cerebral palsy. The upper limb injection goals include improvements in function, better positioning of the arm, and facilitating the ease of care. Neurotoxin type A is the most widely used serotype in the pediatric population. After being injected into muscle, the release of acetylcholine at cholinergic nerve endings is blocked, and a temporary denervation and atrophy ensues. Targeting the correct muscle close to the neuromuscular junctions is considered essential and localization techniques have developed over time. However, each technique has its own limitations. The role of BTXA is flexible, but limited by the temporary mode of action as a focal spasticity treatment and the restrictions on the total dose deliverable per visit. As a mode of treatment, repeated BTXA injections are needed. This literature reviewed BTXA injection techniques, doses and dilutions, the recovery of muscles and the impact of repeated injections, with a focus on the pediatric population. Suggestions for future studies are also discussed.

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