10 The Time Course for the Decline in Miniature End-Plate Potential Frequency Following Tetanic Stimulation of the Motor Nerve

2015 ◽  
pp. 106-118
Author(s):  
Hiroshi Kita ◽  
Kazuhiko Narita ◽  
William Van der Kloot
1968 ◽  
Vol 170 (1021) ◽  
pp. 381-399 ◽  

Exposure of isolated frog skeletal muscle to a cardiac glycoside produces changes in the prejunctional events associated with neuromuscular transmission. The principal changes consist of a progressive increase in the quantum content of the end-plate potential, followed by conduction block in intramuscular motor nerve branches. These events are accompanied by a progressive increase in the frequency of miniature end-plate potentials. Following conduction blockade spontaneous end-plate potentials occur which arise from the generation of action potentials at or near the nerve terminations. Still later, the miniature end-plate potential frequency declines and the nerve endings become entirely inexcitable. These changes appear to result from inhibition of a sodium pump in the motor nerve axons and their endings.


2000 ◽  
Vol 115 (4) ◽  
pp. 519-532 ◽  
Author(s):  
K. Narita ◽  
T. Akita ◽  
J. Hachisuka ◽  
S.-M. Huang ◽  
K. Ochi ◽  
...  

Ca2+-induced Ca2+ release (CICR) enhances a variety of cellular Ca2+ signaling and functions. How CICR affects impulse-evoked transmitter release is unknown. At frog motor nerve terminals, repetitive Ca2+ entries slowly prime and subsequently activate the mechanism of CICR via ryanodine receptors and asynchronous exocytosis of transmitters. Further Ca2+ entry inactivates the CICR mechanism and the absence of Ca2+ entry for >1 min results in its slow depriming. We now report here that the activation of this unique CICR markedly enhances impulse-evoked exocytosis of transmitter. The conditioning nerve stimulation (10–20 Hz, 2–10 min) that primes the CICR mechanism produced the marked enhancement of the amplitude and quantal content of end-plate potentials (EPPs) that decayed double exponentially with time constants of 1.85 and 10 min. The enhancement was blocked by inhibitors of ryanodine receptors and was accompanied by a slight prolongation of the peak times of EPP and the end-plate currents estimated from deconvolution of EPP. The conditioning nerve stimulation also enhanced single impulse- and tetanus-induced rises in intracellular Ca2+ in the terminals with little change in time course. There was no change in the rate of growth of the amplitudes of EPPs in a short train after the conditioning stimulation. On the other hand, the augmentation and potentiation of EPP were enhanced, and then decreased in parallel with changes in intraterminal Ca2+ during repetition of tetani. The results suggest that ryanodine receptors exist close to voltage-gated Ca2+ channels in the presynaptic terminals and amplify the impulse-evoked exocytosis and its plasticity via CICR after Ca2+-dependent priming.


1986 ◽  
Vol 55 (3) ◽  
pp. 551-568 ◽  
Author(s):  
A. Van Boxtel

A comparison was made between the effects of repetition rate, muscle vibration, and tetanic stimulation of the tibial nerve on H-reflexes and tendon (T) jerks elicited in the relaxed soleus muscle of normal human. H- and T-reflexes with electromyographic (EMG) potentials of equivalent amplitude were elicited alternately in the same leg to ensure identical experimental conditions. H- and T-reflexes of identical EMG amplitude showed isometric twitch tensions of identical amplitude and time course. H- and T-reflexes were elicited at different repetition rates ranging from once every 6 s to 2/s. H-reflexes showed a significantly stronger low-frequency depression than T-reflexes. Inhibition of H- and T-reflexes was induced by 2-min vibration at 100 Hz of ankle extensors, ankle flexors, or knee flexors. Vibration of ankle extensors and flexors induced a stronger inhibition than vibration of knee flexors. In all three conditions, inhibition of H-reflexes was stronger than inhibition of T-reflexes. The difference was relatively greater during vibration of ankle extensors and flexors than during vibration of knee flexors. When tested together, the effects of low-frequency depression and vibration-induced inhibition of H- and T-reflexes were found to be independent if reflex amplitudes were expressed as a percentage of the control reflex amplitude. The cessation of vibration of ankle extensors was followed by a gradual recovery of H-reflexes from inhibition. On the contrary, T-reflexes showed a marked potentiation. Such postvibratory effects were generally not observed following vibration of ankle or knee flexors. When postvibratory effects were tested during low-frequency depression, percent postvibratory depression of H-reflexes and percent postvibratory potentiation of T-reflexes were found to be independent of the degree of low-frequency depression. Tetanic stimulation of the tibial nerve for 20 s at 200 Hz resulted in posttetanic potentiation (PTP) of H- and T-reflexes, the former being stronger than the latter. The extent of the changes in H- and T-reflex EMG amplitudes, due to changes in repetition rate, vibration, or tetanic stimulation, was generally inversely related to the intensity of the electrical or mechanical reflex stimuli. The observed discrepancies between the induced changes in H- and T-reflex amplitudes are interpreted in terms of the differences in afferent inputs between the two reflexes that were suggested by Burke and his colleagues (9-11).(ABSTRACT TRUNCATED AT 400 WORDS)


1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.


1993 ◽  
Vol 69 (3) ◽  
pp. 953-964 ◽  
Author(s):  
P. W. Glimcher ◽  
D. L. Sparks

1. The first experiment of this study determined the effects of low-frequency stimulation of the monkey superior colliculus on spontaneous saccades in the dark. Stimulation trains, subthreshold for eliciting short-latency fixed-vector saccades, were highly effective at biasing the metrics (direction and amplitude) of spontaneous movements. During low-frequency stimulation, the distribution of saccade metrics was biased toward the direction and amplitude of movements induced by suprathreshold stimulation of the same collicular location. 2. Low-frequency stimulation biased the distribution of saccade metrics but did not initiate movements. The distribution of intervals between stimulation onset and the onset of the next saccade did not differ significantly from the distribution of intervals between an arbitrary point in time and the onset of the next saccade under unstimulated conditions. 3. Results of our second experiment indicate that low-frequency stimulation also influenced the metrics of visually guided saccades. The magnitude of the stimulation-induced bias increased as stimulation current or frequency was increased. 4. The time course of these effects was analyzed by terminating stimulation immediately before, during, or after visually guided saccades. Stimulation trains terminated at the onset of a movement were as effective as stimulation trains that continued throughout the movement. No effects were observed if stimulation ended 40–60 ms before the movement began. 5. These results show that low-frequency collicular stimulation can influence the direction and amplitude of spontaneous or visually guided saccades without initiating a movement. These data are compatible with the hypothesis that the collicular activity responsible for specifying the horizontal and vertical amplitude of a saccade differs from the type of collicular activity that initiates a saccade.


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