Lüscher H, Ruenzel P W, Henneman E
J Neurophysiol. 1983 Nov;50(5):1045-58. doi: 10.1152/jn.1983.50.5.1045.
Excitatory postsynaptic potentials (EPSPs) were evoked in large populations of motoneurons by impulses in single Ia- and group II fibers and recorded from L7 and S1 ventral roots by means of a sucrose-gap technique and spike-triggered averaging, as previously described (33, 34). Factors known to influence conduction at branch points in peripheral nerves or transmission in the Ia projection to motoneurons were studied to determine their effects on these postsynaptic population potentials (PSPPs). When impulse frequency was plotted against the amplitude of these PSPPs, a sequence of low-frequency depression, higher frequency facilitation, and still higher frequency depression was regularly observed. Similar plots of PSPP amplitude versus impulse frequency in a small sample of group II spindle fibers did not reveal any low-frequency depression. Higher frequency facilitation and depression followed the same pattern as that produced by Ia-fibers. Early potentiation of the PSPPs was produced by applying 20 stimulating pulses at 500/s to branches of the medial gastrocnemius nerves containing single Ia-fibers. Single, posttetanic PSPPs were recorded at fixed intervals following each tetanus and averaged. A brief, initial depression followed by a rapidly declining potentiation of PSPPs was regularly observed. When the core temperature was reduced from 41 to 35 degrees C, there was an approximately linear increase in the amplitude of PSPPs. At each temperature a combination of cooling and posttetanic potentiation (PTP) elicited larger PSPPs than cooling alone. The effects of impulse frequency, PTP, and temperature on PSPPs may all be interpreted in terms of their known effects on action potentials or on conduction at branch points in peripheral nerves. Similar effects on transmission or transmission failure in the terminal arborizations of Ia-fibers would account for the influence of these factors on PSPPs. Alternatively, these same three factors might cause similar effects on PSPPs through influences they might exert on the transmitter release mechanism.
如前所述（33, 34），通过单根Ia纤维和II类纤维的冲动在大量运动神经元中诱发兴奋性突触后电位（EPSP），并采用蔗糖间隙技术和触发尖峰平均法从L7和S1腹根记录。研究了已知影响周围神经分支点传导或Ia纤维向运动神经元投射的传递的因素，以确定它们对这些突触后群体电位（PSPP）的影响。当将冲动频率与这些PSPP的幅度作图时，经常观察到一系列低频抑制、高频易化和更高频率抑制。在一小部分II类肌梭纤维中，PSPP幅度与冲动频率的类似作图未显示任何低频抑制。高频易化和抑制遵循与Ia纤维产生的模式相同的模式。通过以500次/秒的频率向含有单根Ia纤维的内侧腓肠神经分支施加20个刺激脉冲，可产生PSPP的早期增强。在每次强直刺激后以固定间隔记录单个强直后PSPP并进行平均。经常观察到短暂的初始抑制，随后是PSPP迅速下降的增强。当核心温度从41℃降至35℃时，PSPP的幅度大约呈线性增加。在每个温度下，冷却和强直后增强（PTP）的组合比单独冷却引起的PSPP更大。冲动频率、PTP和温度对PSPP的影响都可以根据它们对动作电位或周围神经分支点传导的已知影响来解释。对Ia纤维终末分支的传递或传递失败的类似影响将解释这些因素对PSPP的影响。或者，这三个相同的因素可能通过它们对递质释放机制的影响而对PSPP产生类似的影响。
