首页> 美国卫生研究院文献>The Journal of Neuroscience >Physiological differences between strong and weak frog neuromuscular junctions: a study involving tetanic and posttetanic potentiation
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Physiological differences between strong and weak frog neuromuscular junctions: a study involving tetanic and posttetanic potentiation

机译:强和弱青蛙神经肌肉接头之间的生理差异:涉及强直性和强直性增强的研究

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摘要

This paper describes the extent of release and terminal variability among normal frog sartorius neuromuscular junctions and seeks physiological correlates for these differences. Terminal length varied over approximately a 10-fold range, quantal content and release per unit terminal length (“release efficacy”) over much larger ranges. For purposes of comparison of different junctions, release efficacy in a Ringer's containing 0.25 mM Ca2+ was determined in all cases. In a Ringer's containing 0.1 mM Ca2+, tetanic stimulation causes a buildup of evoked release and of miniature endplate potential (mEPP) frequency. The mEPP frequency at the end of the tetanus is proportional to the evoked release level. Following the tetanus, the mEPP frequency declines in a multiexponential fashion, with the 2 longest decay phases, representing augmentation and posttetanic potentiation (PTP), both having time constants that are positively linearly correlated with the synaptic release efficacy. Longer or higher-frequency tetanic stimulation resulted in a longer time course of decay of mEPP frequency. In a Ca2(+)-free/EGTA Ringer's, tetanic stimulation causes no evoked release, but does lead to an increased mEPP frequency, presumably due to a buildup of free Ca2+ displaced from internal stores by the Na+ influx. Following the tetanus, the mEPP frequency declines to resting level with a time constant that is essentially the same for all junctions, regardless of their release efficacy in Ca2(+)- containing Ringer's. These findings indicate that stronger terminals have a greater influx of Ca2+ per unit length during action potential invasion, but that in the absence of external Ca2+, tetanic stimulation results in comparable release of Ca2+ from internal stores in all terminals and comparable accumulation of Ca2+ in some large compartment, the subsequent emptying of which determines the time course of PTP.
机译:本文描述了正常蛙类赛多利斯神经肌肉接头之间的释放程度和终末变异性,并寻找这些差异的生理相关性。末端长度在大约10倍的范围内变化,定量含量和单位末端长度的释放量(“释放功效”)在更大的范围内变化。为了比较不同的连接点,在所有情况下都确定了在含有0.25 mM Ca2 +的林格氏液中的释放效果。在含有0.1 mM Ca2 +的林格氏液中,强直性刺激会引起诱发的释放和终末板电位(mEPP)频率的累积。破伤风末端的mEPP频率与诱发的释放水平成正比。破伤风之后,mEPP频率以多指数方式下降,具有最长的2个衰减阶段,分别代表增强和破伤风后增强(PTP),它们的时间常数与突触释放功效呈线性正相关。更长或更高频的强直性刺激导致mEPP频率衰减的时间更长。在无Ca2 +的/ EGTA林格氏症中,强直性刺激不会引起诱发的释放,但确实会导致mEPP频率增加,这可能是由于Na +涌入从内部存储中置换出的游离Ca2 +堆积所致。破伤风后,mEPP频率下降到静止水平,其时间常数对于所有路口基本相同,无论它们在含Ca2 +的林格氏液中的释放功效如何。这些发现表明,较强的末端在动作电位入侵期间每单位长度的Ca2 +流入量更大,但是在没有外部Ca2 +的情况下,强直性刺激会导致所有末端的内部存储中Ca2 +的释放量相当,而在某些情况下,Ca2 +的累积量也相当。大隔间,随后的排空决定了PTP的时间进程。

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