Binomial distribution analysis of one component of the short-term synaptic plasticity, facilitation, at the frog neuromuscular junction

2011 ◽  
Vol 71 ◽  
pp. e112
Author(s):  
Naoya Suzuki ◽  
Kazumasa Fushimi
Keyword(s):  
Synaptic Plasticity ◽  
Neuromuscular Junction ◽  
Binomial Distribution ◽  
Frog Neuromuscular Junction ◽  
Distribution Analysis ◽  
Short Term

scholarly journals New insights into short-term synaptic facilitation at the frog neuromuscular junction

2015 ◽  
Vol 113 (1) ◽  
pp. 71-87 ◽  
Author(s):  
Jun Ma ◽  
Lauren Kelly ◽  
Justin Ingram ◽  
Thomas J. Price ◽  
Stephen D. Meriney ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Binding ◽  
High Frequency Stimulation ◽  
Frog Neuromuscular Junction ◽  
Short Term ◽  
Calcium Binding Site ◽  
Synaptic Facilitation ◽  
Site Model ◽  
Computer Simulation Studies ◽  
Sensor Proteins

Short-term synaptic facilitation occurs during high-frequency stimulation, is known to be dependent on presynaptic calcium ions, and persists for tens of milliseconds after a presynaptic action potential. We have used the frog neuromuscular junction as a model synapse for both experimental and computer simulation studies aimed at testing various mechanistic hypotheses proposed to underlie short-term synaptic facilitation. Building off our recently reported excess-calcium-binding-site model of synaptic vesicle release at the frog neuromuscular junction (Dittrich M, Pattillo JM, King JD, Cho S, Stiles JR, Meriney SD. Biophys J 104: 2751–2763, 2013), we have investigated several mechanisms of short-term facilitation at the frog neuromuscular junction. Our studies place constraints on previously proposed facilitation mechanisms and conclude that the presence of a second class of calcium sensor proteins distinct from synaptotagmin can explain known properties of facilitation observed at the frog neuromuscular junction. We were further able to identify a novel facilitation mechanism, which relied on the persistent binding of calcium-bound synaptotagmin molecules to lipids of the presynaptic membrane. In a real physiological context, both mechanisms identified in our study (and perhaps others) may act simultaneously to cause the experimentally observed facilitation. In summary, using a combination of computer simulations and physiological recordings, we have developed a stochastic computer model of synaptic transmission at the frog neuromuscular junction, which sheds light on the facilitation mechanisms in this model synapse.

scholarly journals Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels

2016 ◽  
Vol 113 (4) ◽  
pp. 1068-1073 ◽  
Author(s):  
Evanthia Nanou ◽  
Jin Yan ◽  
Nicholas P. Whitehead ◽  
Min Jeong Kim ◽  
Stanley C. Froehner ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Muscle Strength ◽  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Motor Coordination ◽  
Tibialis Anterior Muscle ◽  
Short Term ◽  
Synaptic Facilitation ◽  
Cas Proteins

Facilitation and inactivation of P/Q-type calcium (Ca2+) currents through the regulation of voltage-gated Ca2+ (CaV) 2.1 channels by Ca2+ sensor (CaS) proteins contributes to the facilitation and rapid depression of synaptic transmission in cultured neurons that transiently express CaV2.1 channels. To examine the modulation of endogenous CaV2.1 channels by CaS proteins in native synapses, we introduced a mutation (IM-AA) into the CaS protein-binding site in the C-terminal domain of CaV2.1 channels in mice, and tested synaptic facilitation and depression in neuromuscular junction synapses that use exclusively CaV2.1 channels for Ca2+ entry that triggers synaptic transmission. Even though basal synaptic transmission was unaltered in the neuromuscular synapses in IM-AA mice, we found reduced short-term facilitation in response to paired stimuli at short interstimulus intervals in IM-AA synapses. In response to trains of action potentials, we found increased facilitation at lower frequencies (10–30 Hz) in IM-AA synapses accompanied by slowed synaptic depression, whereas synaptic facilitation was reduced at high stimulus frequencies (50–100 Hz) that would induce strong muscle contraction. As a consequence of altered regulation of CaV2.1 channels, the hindlimb tibialis anterior muscle in IM-AA mice exhibited reduced peak force in response to 50 Hz stimulation and increased muscle fatigue. The IM-AA mice also had impaired motor control, exercise capacity, and grip strength. Taken together, our results indicate that regulation of CaV2.1 channels by CaS proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo.

Presynaptic effects of a trinitrobenzene analogue at the frog neuromuscular junction

1996 ◽  
Vol 76 (3) ◽  
pp. 1735-1743 ◽  
Author(s):  
M. Osanai ◽  
A. Tsuji ◽  
N. Suzuki ◽  
H. Kijima
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Time Course ◽  
Control Level ◽  
Protein S ◽  
Specific Protein ◽  
Frog Neuromuscular Junction ◽  
Short Term ◽  
Similar Time ◽  
Presynaptic Nerve Terminal

1. Application of 0.15 mM 1-(hydroxyethylamino)-2,4,6-trinitrobenzene (HEATNB) to the frog neuromuscular junction induced a marked increase (4.0-fold) in the amplitude of nerve-evoked end-plate potentials (EPPs) obtained from intracellular and extracellular records, but only a slight increase (1.9-fold) in the frequency of miniature EPPs (MEPPs) obtained from intracellular records. The effects of HEATNB on EPP amplitude and MEPP frequency showed a similar time course, reaching a plateau level approximately 40 min after the start of application and returning to the control level after wash. The difference in the effects of HEATNB on EPP and MEPP frequency suggests that it specifically enhances synchronous transmitter release. 2. Comparing the effects and structure of HEATNB with those of 2,4,6-trinitrobenzene-1-sulfonic acid, we conclude that the observed increase in transmitter release is due to the effects of the trinitrobenzene moiety of those reagents. 3. The distribution of MEPP amplitude was unchanged by HEATNB treatment, indicating that its effects are presynaptic. 4. Among four components of short-term synaptic plasticity, HEATNB greatly decreased (approximately 70%) augmentation and increased (approximately 50%) potentiation, but had little effect on fast and slow facilitations. These results suggest that each of the short-term plasticities has a different mechanism and that HEATNB affects the same mechanisms as those of augmentation. 5. Even when a calcium chelator, bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid, was loaded into the presynaptic nerve terminal, the effects of HEATNB were not changed in nature, suggesting that effects of HEATNB persist independently of intracellular Ca2+ concentration. 6. These observations suggest that HEATNB may affect specific protein(s) involved primarily in synchronous transmitter release and not asynchronous release.

scholarly journals Computer simulation of free Ca^ and synaptic plasticity at the presynaptic terminal of frog neuromuscular junction

1999 ◽  
Vol 39 (supplement) ◽  
pp. S52
Author(s):  
M. Murase ◽  
K. Ito ◽  
S. Suzuki ◽  
T. Kazawa ◽  
N. Suzuki ◽  
...  
Keyword(s):  
Computer Simulation ◽  
Synaptic Plasticity ◽  
Neuromuscular Junction ◽  
Presynaptic Terminal ◽  
Frog Neuromuscular Junction
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