Taylor C P, Dudek F E
J Neurophysiol. 1984 Jul;52(1):126-42. doi: 10.1152/jn.1984.52.1.126.
The effects of electrical fields from antidromic stimulation of CA1 pyramidal cells were studied in slices of rat hippocampus in which chemical synaptic transmission had been blocked by superfusion with physiological solution containing Mn2+ and lowered concentration of Ca2+. Differential voltage recordings were made between two microelectrode positions, on intracellular to a pyramidal cell and the other in the adjacent extracellular space. This technique revealed brief transmembrane depolarizations that occurred synchronously with negative-going extracellular population spikes in the adjacent cell body layer. Glial cells in this region did not exhibit these depolarizations. In some pyramidal cells, alvear stimulation that was too weak to excite the axon of the impaled cell elicited action potentials, which appeared to arise from transmembrane depolarizations at the soma. When subthreshold transmembrane depolarizations were superimposed on subthreshold depolarizing current pulses, somatic action potentials were generated synchronously with the antidromic population spikes. The depolarizations of pyramidal somata were finely graded with stimulus intensity, were unaffected by polarization of the membrane, and were not occluded by preceding action potentials. The laminar profile of extracellular field potentials perpendicular to the cell body layer was obtained with an array of extracellular recording locations. Numerical techniques of current source-density analysis indicated that at the peak of the somatic population spike, there was an extracellular current sink near pyramidal somata and sources in distal dendritic regions. It is concluded that during population spikes an extracellular electrical field causes currents to flow passively across inactive pyramidal cell membranes, thus depolarizing their somata. The transmembrane depolarizations associated with population spikes would tend to excite and synchronize the population of pyramidal cells.
在大鼠海马切片中研究了对CA1锥体细胞进行逆向刺激产生的电场效应，其中化学突触传递已通过用含Mn2+且降低Ca2+浓度的生理溶液进行灌流而被阻断。在两个微电极位置之间进行差分电压记录，一个位于锥体细胞内，另一个位于相邻的细胞外空间。该技术揭示了与相邻细胞体层中负向细胞外群体锋电位同步发生的短暂跨膜去极化。该区域的胶质细胞未表现出这些去极化。在一些锥体细胞中，强度太弱以至于无法激发被穿刺细胞轴突的肺泡刺激引发了动作电位，这些动作电位似乎源于胞体处的跨膜去极化。当阈下跨膜去极化叠加在阈下去极化电流脉冲上时，体细胞动作电位与逆向群体锋电位同步产生。锥体细胞胞体的去极化随刺激强度精细分级，不受膜极化影响，且不会被先前的动作电位所阻断。通过一系列细胞外记录位置获得了垂直于细胞体层的细胞外场电位的层状分布。电流源密度分析的数值技术表明，在体细胞群体锋电位的峰值处，锥体细胞胞体附近存在细胞外电流汇，而在远端树突区域存在电流源。得出的结论是，在群体锋电位期间，细胞外电场使电流被动地流过无活性的锥体细胞膜，从而使其胞体去极化。与群体锋电位相关的跨膜去极化倾向于激发锥体细胞群体并使其同步。
