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 mu-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.
The aim of the study was to test the hypothesis that a 16 week endurance training program would alter the abundance of endplate-associated nicotinic acetylcholine receptors (nAChR) in various rat skeletal muscles. We found a 20% increase in endplate-specific [125I]alpha-bungarotoxin binding in several muscles of trained rats, accompanied by equal susceptibility of toxin binding to the inhibitory effect of D-tubocurarine in sedentary and trained muscles. We conclude that the neuromuscular junction adaptations that occur with increased chronic activation include an increase in nAChR number. Results of experiments designed to determine nAChR turnover also suggest that this effect is mediated by an alteration in the receptor's metabolic state. The potential implications and mechanisms of this adaptation are discussed.
To better understand the effect of muscle hypertrophy on the physiological properties of transmitter release, we investigated neuromuscular transmission (NMT) efficacy in overloaded rat plantaris muscle in situ. In the overload group, following bilateral tenotomy of plantaris synergists, rats were confined to wheel-cages. Age-matched rats in the control group were confined to plastic cages. During the terminal experiment, muscle action potentials were blocked using micro-conotoxin, and full-sized endplate potentials (EPPs) were recorded at 25, 50, and 75 HZ to determine their amplitude rundown. Quantal contents for the control and overload groups were 37.0 and 74.3, respectively (P <0.01). There was a significant group difference in EPP amplitude rundown at all frequencies examined, with increased rundown occurring in the overload group (P < 0.01). Cumulative quantal release was 139% and 153% higher in the overload group at 25 and 50 HZ, respectively (P < 0.05). Together, these data suggest the safety factor for NMT is increased by neuromuscular overload. Furthermore, these findings support and supplement previously reported activity-dependent improvements in NMT efficacy that are probably mediated via presynaptic adaptations.
Studies dealing with neuromuscular transmission efficacy typically employ continuous patterns of activation to demonstrate decrements in endplate potential (epp) amplitude. Recent evidence from rat diaphragm muscle has shown that including periods of quiescence to the stimulation protocol allows epp amplitude to recover between series of contractions. Whether similar recovery occurs in rat hindlimb muscle is unknown. In this study, we have measured declines in epp amplitude in rat soleus muscle during trains of stimulation evoked either continuously (10 s) or intermittently (400 ms repeated every second), using an in situ approach. As in diaphragm, we found that rest periods within the intermittent trains significantly improved neuromuscular transmission efficacy. However, unlike the diaphragm, epp amplitude recovery was incomplete even by the second train in the intermittent protocols, recovery being frequency-dependent and ranging from 40 to 50%. The results suggest that the kinetics of epp amplitude rundown and recovery may be muscle-specific, and should be considered when evaluating situations in which neuromuscular transmission efficacy may be altered.
Increased neuromuscular activity is known to provoke morphological and functional adaptations at the neuromuscular synapse. Most of these changes have been documented following endurance exercise training programmes. In this study, the effect of rat soleus muscle overload produced by tenotomy plus voluntary wheel-cage activity on neuromuscular transmission efficacy was investigated. The overload protocol increased miniature endplate potential (MEPP) and endplate potential (EPP) amplitudes by 17 and 19%, respectively (both P < 0.01), and increased MEPP frequency by 86% (P < 0.01). EPP amplitude rundown during continuous trains of activation was attenuated by ∼10% in the overloaded group (P < 0.01). Also, during intermittent activation, the overload protocol attenuated EPP amplitude rundown, mainly by enhancing EPP amplitude recovery by ∼10% during the quiescent periods (P < 0.01). Although the present results show that both the degree and direction of adaptation are similar to what has been observed at rat soleus neuromuscular junctions following an endurance training protocol, there are important nuances between the results, suggesting different mechanisms through which these changes may occur.
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