854 



HANDBOOK OF I'insioLor; V 



NEI'ROPHVSIOLOGY II 



FIG. 1 7. Response of Betz cells to threshold and suprathresh- 

 old antidromic pyramidal shocks in cats under chloralose- 

 decamethonium anesthesia. Left column, unit responses; right 

 column, surface responses (area I). Upper. Response to threshold 

 stimulus (o.oi msec, pulse) to bulbar pyramid; single spike on 

 left followed repetition rates of 100 per sec. (not shown). Middle. 

 Responses to suprathreshold (0.04 msec, pulse) pyramidal shock ; 

 only first of three spikes in left figure followed 100 per sec. stimu- 

 lus rates (not shown). Lower. Shock to contralateral forepaw 

 precedes suprathreshold pyramidal shock ; note in test responses 

 that late spikes are blocked and late surface dettcction attenuated. 

 Time, 2 msec. (From Patton & Towe, unpublished observa- 

 tions.) 



many units splitting cannot be demonstrated even 

 with stimulation rates up to 200 to 300 per sec. 

 Phillips observed the inflection in 7 of 16 cells. 



Unfortunately, Phillips did not study orthodromic 

 excitation of Betz cells, but his figure 4 shows spikes 

 elicited in a unit (not a Betz cell) by a strong shock to 

 the pyramid which clearly exerted its effect by spread 

 to the medial lemniscus. The spike arises from a slowly 

 developing prepotential similar to that observed in 

 intracellular recordings from orthodromically excited 

 motoneurons (see also 4, fig. i). Also, in spontaneoush- 

 arising trains, spikes were preceded by slow depolari- 

 zation which was abolished by the spike only to build 

 up again to the firing level which varied only within 

 narrow limits. 



Following a spike (antidromic or spontaneous), the 



membrane potential often showed an increase which 

 decayed o\'er a period of about 50 msec. Phillips 

 ascribed this postspike hyperpolarization to inhil^itory 

 action of recurrent axon collaterals, comparaljle to 

 that described for spinal motoneurons (32); but on the 

 basis of evidence discussed below, this explanation 

 must be rejected. It is more probable that the post- 

 spike hyperpolarization is comparable to that de- 

 scril)cd in the lightly stretched stretch receptor of 

 crustaceans (34) where there are no recurrent col- 

 laterals. In the latter instance, hyperpolarization 

 (relative to the prespike memljrane potential) results 

 when the antidromic spike invades the slowly conduct- 

 ing dendrites. The depolarizing effect of the dendritic 

 generator potential on cell body membrane potential 

 is probably reduced either because the potassium 

 permeability of the cell body is increased during 

 recovery or because the generator potential is tem- 

 porarily ol:)llterated after the spike invades the genera- 

 tor region. Similar postspike hyperpolarization has 

 been described in other excitable structures in which 

 membrane potential was reduced prior to firing. In 

 Phillips" experiments on lightly anesthetized animals, 

 some depolarization of cells was suggested by the 

 spontaneous firing and by membrane potentials lower 

 than expected for 'resting' neurons. That the apical 

 dendrites of Betz cells, like the dendritic terminals of 

 crustacean stretch receptors (33, 34, 48), are sites of 

 nonpropagated generator potentials which bias the 

 excitability of the cell body (23) remains to be proved, 

 but has been ably and convincingly argued by Clare 

 & Bishop whose papers (28, 29) may be consulted for 

 summary and references. 



Extracellularly recorded spikes of Betz cells (figs. 13, 

 17, 18) do not differ significantly from similarly re- 

 corded spikes of other cortical cells (3, 66, 67) ; they 

 are usually positive-negative, occasionally negative. 

 Antidromic spikes are often indistinguishable from 

 orthodromically elicited spikes, but occasionally 

 there are minor differences, as in figure 18 in which 

 the antidromic spikes are consistently of greater ampli- 

 tude than the orthodromic. 



RECURRENT .\XON COLL.\TER.\LS OF BETZ CELLS 



The axons of Betz cells give off a profusion of 

 collateral branches within the gray matter (23, 74, 88). 

 Axon collaterals of cells in the internal lamina not 

 only ramify within layers V and \\ but course up- 

 ward to branch among the cells of layers III, II and 

 even I. Layer I\' apparently receives few axon col- 



