Lev-Tov A, Pinter M J, Burke R E
J Neurophysiol. 1983 Aug;50(2):379-98. doi: 10.1152/jn.1983.50.2.379.
We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group Ia monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) alpha-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Lüscher and colleagues (43, 44) of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (Pmax) and 1) the mean amplitude of the pretetanic control EPSP in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as "differential distribution of PTP" within the MG motor pool, were less strong in the present work than reported by Lüscher et al. (43, 44). We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of Pmax subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as "specific" synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the nonlinear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.
我们重新研究了戊巴比妥麻醉猫的内侧腓肠肌（MG）α运动神经元中Ia类单突触兴奋性突触后电位（EPSP）的强直后增强（PTP）现象。结果总体上证实了吕舍尔及其同事早期的报告（43, 44），即Ia EPSP幅度的最大增强百分比（Pmax）与以下两者之间呈负相关：1）同一细胞中强直前对照EPSP的平均幅度；2）突触后运动神经元的输入电阻。我们将这些负相关称为MG运动池中“PTP的差异分布”，在本研究中，这些负相关不如吕舍尔等人报告的（43, 44）那么强烈。我们还发现，通过第一个强直后EPSP的幅度评估的强直后EPSP抑制与随后达到的Pmax水平之间存在相对较强的负相关。我们没有发现证据表明强直后抑制是由突触前动作电位失败引起的。我们研究了第二种类型的抑制，称为“特异性”突触抑制，其中配对反应（间隔250毫秒）的第二个EPSP的峰值幅度平均比第一个EPSP小。这种现象似乎反映了先前激活的突触释放递质的概率降低。当配对反应由高频强直刺激调节时，特异性突触抑制持续增加。这最容易通过假设PTP至少部分是由于Ia类突触释放递质的统计概率增加来解释，这些突触在传入强直刺激前后均被激活（即可能被动作电位侵入）。根据目前的结果和其他现有证据，我们得出结论，PTP的差异分布可以由两个主要因素来解释：1）所有化学突触中固有的电导与电压变化之间的非线性关系；2）支配不同运动神经元的Ia类突触特性的系统变化，这仍有待阐明。
