Baker R, Llinás R
J Physiol. 1971 Jan;212(1):45-63. doi: 10.1113/jphysiol.1971.sp009309.
Electrical stimulation of the trigeminal nerve evokes a ;short latency depolarization' (SLD) in the first order sensory neurones of the mesencephalic nucleus (MSN) of the Vth nerve in the rat. A series of experiments suggesting ;electrotonic coupling' as the mechanism for this SLD is provided.1. Electrical activity of MSN neurones was recorded intracellularly as action potentials were conducted from the periphery (somatopetally) to the masticatory nucleus. Typical sequential invasion of the initial segment and somatic region (IS-S) of the neurones was seen. The somatopetal activation of MSN neurones was characterized by the brevity, short refractoriness, high safety factor (IS-S), and short after-hyperpolarization of the spike potential.2. In twenty-three (10.5%) of the penetrated neurones, stimulation at levels subthreshold for somatopetal activation uncovered a SLD with a mean latency of 180 musec.3. The SLDs were found to be all-or-none in nature, and to have constant amplitude and latency for a given cell, plus a short half decay time.4. Hyperpolarization of a MSN neurone through the recording electrode produced a blockage of the IS-S spike and revealed M-spikes and SLDs which could be clearly separated, in every instance, as distinct all-or-none components. The amplitude of the SLD was found to be insensitive to the level of membrane potential within the ranges tested.5. In fifteen neurones the SLD generated action potentials which were conducted somatofugally as shown by their collision with somatopetally conducted action potentials in the same cell. The lack of collision between the SLD and somatopetal spikes demonstrated the independent origin of these two potentials.6. The independence of the SLD from the somatopetal invasion of the cell was also demonstrated by collision of a somatofugal action potential following direct stimulation through the recording micro-electrode and a somatopetal spike following trigeminal stimulation.7. Two possible mechanisms are considered for the genesis of the SLD: chemical synaptic transmission and electrotonic coupling between neighbouring cells. The conclusion is drawn that SLDs must be generated by the latter mechanism.
电刺激大鼠三叉神经会在其第五对脑神经中脑核(MSN)的一级感觉神经元中诱发一种“短潜伏期去极化”(SLD)。本文提供了一系列实验,表明“电紧张性耦合”是这种SLD的产生机制。1. 在将动作电位从外周(向心性)传导至咀嚼核的过程中,细胞内记录了MSN神经元的电活动。观察到神经元的起始段和胞体区域(IS-S)典型的顺序性兴奋。MSN神经元的向心性激活具有动作电位短暂、不应期短、安全系数高(IS-S)以及锋电位后超极化时间短的特点。2. 在23个(10.5%)被穿透的神经元中,在低于向心性激活阈值的水平进行刺激时,发现了平均潜伏期为180微秒的SLD。3. 发现SLD本质上具有全或无的特性,对于给定的细胞,其幅度和潜伏期恒定,且半衰期短。4. 通过记录电极对MSN神经元进行超极化会导致IS-S锋电位受阻,并揭示出M锋电位和SLD,在每种情况下,它们都可作为明显的全或无成分清晰分离。发现在测试范围内,SLD的幅度对膜电位水平不敏感。5. 在15个神经元中,SLD产生的动作电位以离心性方式传导,这可通过它们与同一细胞中向心性传导的动作电位发生碰撞得以证明。SLD与向心性锋电位之间没有碰撞,证明了这两种电位的起源相互独立。6. 通过记录微电极直接刺激后产生的离心性动作电位与三叉神经刺激后产生的向心性锋电位发生碰撞,也证明了SLD与细胞向心性兴奋的独立性。7. 考虑了SLD产生的两种可能机制:化学性突触传递和相邻细胞之间的电紧张性耦合。得出的结论是,SLD必定是由后一种机制产生的。