THE PYRAMIDAL TRACT: ITS EXCITATION AND FUNCTIONS 



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MEAN INITIAL LATENCY (msec.) I""ei: ' 



FIG. 16. Left. Graph showing initial spike latency of cortical cells isolated at different depths 

 from the surface of cortex in chloralose-anesthetizcd cats. Roman numerals on the ordinate also show 

 average extents of cytoarchitectural layers. All cells isolated in arm area I and fired by shock to 

 contralateral footpad. Betz cells denoted by crosses; other cells by dots. Right. Mean initial latencies 

 of units isolated in difTerent cytoarchitectural layers. .Numbers to the left of points indicate number 

 of units; bracketed figures to the right, standard deviations of the means. Numbers between points give 

 probability that the null hypothesis is correct. (From Patton & Towe, unpublished observations.) 



latencies of Betz cells in the different layers may re- 

 flect synaptic spread downward from layers III and 

 IV, but the differences are too small and the variation 

 too great to permit the drawing of definite conclusions. 



BETZ CELL SPIKE 



Another means of investigating the excitation of 

 Betz cells is intracellular recording of spike potentials, 

 a method of proved value in similar studies on spinal 

 motoneurons. Unfortunately, the application of this 

 useful technique to cortical cells is much more difficult 

 than experience with spinal motoneurons would sug- 

 gest (4, 66, 97). Despite repeated attempts, the 

 authors ha\e succeeded only rarely in obtaining 

 satisfactory intracellular recordings from cortical 

 neurons. Cortical movements due to respiration and 

 pulse, even when reduced to a minimum by pneumo- 

 thorax, cisternal drainage and the use of a plate 

 pressed on the cortex (3), are serious handicaps. In 

 addition, cortical cells appear to be more fragile than 

 their spinal cousins, and penetration (indicated by 

 d.c. shift) is usually accompanied by the familiar, 

 agonizing, injury squeal followed by dismal silence. 

 That movement is only partly responsible is suggested 



by the fact that extracellular spikes of amplitudes (10 

 to 20 mv) compatible with close proximity of the 

 electrode and the cell membrane may be recorded for 

 an hour or more withovit deterioration or indication 

 of injury. 



To Phillips (85) goes the credit for obtaining the 

 first significant series of intracellular recordings from 

 Betz cells. In 69 experiments on cats anesthetized 

 with hexobarbitone, he successfully penetrated 16 

 Betz cells maintained in an excitable state for periods 

 of 5 to 40 min. Membrane potentials ranged from 48 

 to 69 mv; spike amplitudes (antidromically evoked by 

 pyramidal stimulation), from 45 to 84 mv, with over- 

 shoots ranging from —17 to -f20 mv. The anti- 

 dromic spike often displayed an inflection on the 

 rising phase, suggesting delayed conduction over 

 regions of low safety factor similar to that observed in 

 motoneurons (15). In extracellular recordings, Patton 

 & Towe (unpublished obser\ationsj observed inflec- 

 tion points on the descending liinl) of positive-negative 

 spikes. These inflections sometimes split off into pure 

 positive deflections of reduced amplitude during high- 

 frequency antidromic stimulation. The most probable 

 point for such blockage is the axon-soma junction (23), 

 but conduction through this region seems to be less 

 tenuous in Betz cells than in motoneurons because in 



