Incomplete recovery of endplate potential amplitude while intermittently activating rat soleus neuromuscular junctions in situ

2002 ◽  
Vol 26 (6) ◽  
pp. 810-816 ◽  
Author(s):  
Patrice Desaulniers ◽  
Pierre-Andr� Lavoie ◽  
Phillip F. Gardiner
Keyword(s):  
Neuromuscular Junctions ◽  
Potential Amplitude ◽  
Endplate Potential

Habitual exercise enhances neuromuscular transmission efficacy of rat soleus muscle in situ

2001 ◽  
Vol 90 (3) ◽  
pp. 1041-1048 ◽  
Author(s):  
Patrice Desaulniers ◽  
Pierre-André Lavoie ◽  
Phillip F. Gardiner
Keyword(s):  
Soleus Muscle ◽  
Neuromuscular Transmission ◽  
Motor Nerve ◽  
Resting Membrane Potential ◽  
Potential Amplitude ◽  
Endplate Potential ◽  
Habitual Exercise ◽  
Rat Soleus Muscle ◽  
Miniature Endplate Potential

Rat motor nerve terminals and the endplates they interact with exhibit changes to varying patterns of use, as when exposed to increased activation in the form of endurance exercise training. The extent to which these changes affect neuromuscular transmission efficacy is uncertain. In this study, the effects of habitual exercise on the electrophysiological properties of neuromuscular transmission in rat soleus muscle were investigated using a novel in situ approach. Consistent with previous reports, miniature endplate potential frequency was enhanced by habitual exercise. Other passive properties, such as resting membrane potential, miniature endplate potential amplitude, and “giant” miniature endplate potential characteristics were unaltered by the training program. Full-size endplate potentials were obtained by blocking soleus muscle action potentials with μ-conotoxin GIIIb. Quantal content values were 91.5 and 119.9 for control and active groups, respectively ( P < 0.01). We also measured the rate and extent of endplate potential amplitude rundown during 3-s trains of continuous stimulation at 25, 50, and 75 Hz; at 50 and 75 Hz, we found both the rate and extent of rundown to be significantly attenuated (10–20%) in a specific population of cells from active rats ( P < 0.05). The results establish the degree of activity-dependent plasticity as it pertains to neuromuscular transmission in a mammalian slow-twitch muscle.

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.

scholarly journals Localization of nicotinic acetylcholine receptor alpha-subunit transcripts during myogenesis and motor endplate development in the chick.

1989 ◽  
Vol 108 (3) ◽  
pp. 1025-1037 ◽  
Author(s):  
B Fontaine ◽  
J P Changeux
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Muscle Development ◽  
Neuromuscular Junctions ◽  
Primary Cultures ◽  
Motor Endplate ◽  
Alpha Subunit ◽  
Subunit Gene ◽  
Nicotinic Acetylcholine

In 15-d-old chick latissimi dorsi muscles, the nicotinic acetylcholine receptor (AChR) alpha-subunit mRNA is densely accumulated at the level of subsynaptic nuclei of the motor endplate (Fontaine et al., 1988). In this paper, using in situ hybridization with genomic probes, we further show that the expression of the AChR alpha-subunit gene in the embryo, revealed by the accumulation of mature mRNAs, starts in myotomal cells and persists during the first stages of muscle development in a majority of muscle nuclei. Subsequently, the distribution of AChR alpha-subunit mRNAs becomes restricted to the newly formed motor endplates as neuromuscular junctions develop. To assess the transcriptional activity of individual nuclei in developing muscles, a strictly intronic fragment of the AChR alpha-subunit gene was used to probe in situ the level of unspliced transcripts. AChR alpha-subunit unspliced transcripts accumulate around a large number of sarcoplasmic nuclei at embryonic day 11, but can no longer be detected at their level after embryonic day 16 in the embryo. A similar decrease in the accumulation of AChR alpha-subunit transcripts is observed between day 4 and day 6 in primary cultures of muscle cells. On the other hand, in vivo denervation and in vitro blocking of muscle electrical activity by the sodium channel blocker tetrodotoxin results in an increase in the labeling of muscle nuclei. Yet, only 6% of the muscle nuclei appear labeled by the strictly intronic probes after denervation. The possible significance of such heterogeneity of muscle nuclei during motor endplate formation in AChR gene expression is discussed.

Neuromuscular Facilitation in Crayfish: Dependence on Potassium and Strophanthidin

1980 ◽  
Vol 86 (1) ◽  
pp. 39-47
Author(s):  
C. LEO ORTIZ ◽  
R. K. ORKAND
Keyword(s):  
Neuromuscular Junctions ◽  
Short Term ◽  
Presynaptic Terminals ◽  
Potential Amplitude ◽  
Junctional Potential ◽  
Long Term Facilitation

1. Long-term facilitation (LTF) and short-term facilitation (STF) at excitatory neuromuscular junctions were studied under conditions of varying [K+]0 and with the addition of strophanthidin. 2. The magnitude of LTF varied inversely with [K+]0, while STF was unaffected. 3. Strophanthidin concentrations greater than 10−5 M greatly increased LTF, but not STF. 4. Both LTF and STF were unaffected by large decreases in excitatory junctional potential amplitude produced by the addition of GABA or Mn+2. 5. The results support the hypothesis that LTF is a consequence of Na+ accumulation in presynaptic terminals and behaves independently of STF.

scholarly journals Endomicroscopy and electromyography of neuromuscular junctions in situ

2014 ◽  
Vol 1 (11) ◽  
pp. 867-883 ◽  
Author(s):  
Rosalind Brown ◽  
Kosala N. Dissanayake ◽  
Paul A. Skehel ◽  
Richard R Ribchester
Keyword(s):  
Neuromuscular Junctions

scholarly journals Changes in the structure of neuromuscular junctions caused by variations in osmotic pressure.

1976 ◽  
Vol 69 (3) ◽  
pp. 521-538 ◽  
Author(s):  
A W Clark
Keyword(s):  
Osmotic Pressure ◽  
Synaptic Vesicles ◽  
Rana Pipiens ◽  
Neuromuscular Junctions ◽  
Presynaptic Membrane ◽  
Normal Position ◽  
Structural Modifications ◽  
Endplate Potential ◽  
Miniature Endplate Potential ◽  
Potential Frequency

Neuromuscular junctions of the frog, Rana pipiens, were examined for structural modifications produced by exposure to increased and reduced osmotic pressure (pi). Preparations exposed to increased pi for varying lengths of time were fixed with either OSO4-Veronal with and without calcium, glutaraldehyde-phosphate, or glutaraldehyde-formaldehyde-phosphate as primary fixatives. The greatest difference between the fixatives was seen in preparations exposed to increased pi for 5 min, corresponding to the time when miniature endplate potential frequency is highest. The 5-min OSO4 calcium-free preparations appeared comparatively normal, while those fixed with OSO4 and 2 mM CaCl2 or aldehyde-phosphate had wide infoldings of the presynaptic membrane and a reduced number of synaptic vesicles. Aldehyde-phosphate had the same effect on mouse diaphragm. Another series of frog preparations were conditioned to elevated pi and then returned to normal Ringer's for varying times before fixation in OSO4-phosphate. Preparations fixed 2 min after their return to normal Ringer's showed marked disruption of the presynaptic membrane as well as apparently rupturing vesicles. If fixed after 10 min, terminals were depleted of vesicles although the presynaptic membrane had returned to its normal position and appearance.

scholarly journals Confocal Endomicroscopy of Neuromuscular Junctions Stained with Physiologically Inert Protein Fragments of Tetanus Toxin

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1499
Author(s):  
Cornelia Roesl ◽  
Elizabeth R. Evans ◽  
Kosala N. Dissanayake ◽  
Veronika Boczonadi ◽  
Ross A. Jones ◽  
...  
Keyword(s):  
Tetanus Toxin ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Full Length ◽  
Nerve Terminals ◽  
Motor Nerve Terminals ◽  
Mouse Muscle ◽  
Confocal Endomicroscopy ◽  
Derivatives Of

Live imaging of neuromuscular junctions (NMJs) in situ has been constrained by the suitability of ligands for inert vital staining of motor nerve terminals. Here, we constructed several truncated derivatives of the tetanus toxin C-fragment (TetC) fused with Emerald Fluorescent Protein (emGFP). Four constructs, namely full length emGFP-TetC (emGFP-865:TetC) or truncations comprising amino acids 1066–1315 (emGFP-1066:TetC), 1093–1315 (emGFP-1093:TetC) and 1109–1315 (emGFP-1109:TetC), produced selective, high-contrast staining of motor nerve terminals in rodent or human muscle explants. Isometric tension and intracellular recordings of endplate potentials from mouse muscles indicated that neither full-length nor truncated emGFP-TetC constructs significantly impaired NMJ function or transmission. Motor nerve terminals stained with emGFP-TetC constructs were readily visualised in situ or in isolated preparations using fibre-optic confocal endomicroscopy (CEM). emGFP-TetC derivatives and CEM also visualised regenerated NMJs. Dual-waveband CEM imaging of preparations co-stained with fluorescent emGFP-TetC constructs and Alexa647-α-bungarotoxin resolved innervated from denervated NMJs in axotomized WldS mouse muscle and degenerating NMJs in transgenic SOD1G93A mouse muscle. Our findings highlight the region of the TetC fragment required for selective binding and visualisation of motor nerve terminals and show that fluorescent derivatives of TetC are suitable for in situ morphological and physiological characterisation of healthy, injured and diseased NMJs.

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