56 J. C. ECCLES 



Eccles, Eccles and Magni, 1960) that every feature of the e.p.s.p. depression is 

 fully explicable by the demonstrated presynaptic depolarization, which would 

 be effective by its action in depressing the size of the presynaptic impulse and 

 hence decreasing the liberation of excitatory transmitter substance. Such an 

 action appears to be demonstrated in the investigation of Hagiwara and 

 Tasaki (1958) on the squid stellate ganglion. 



Presynaptic depolarization of group la afferent fibres has been demonstrated 

 both by the increased excitability exhibited to brief testing pulses applied 

 through a microelectrode in the immediate proximity of the presynaptic 

 terminals in the motoneuron nucleus (Fig. 7a-i) and by the generation of 

 impulses in the la presynaptic fibres which are observed to be discharged 

 along these fibres as a dorsal root reflex (Fig. 6d, e), particularly when the 

 animal is cool (about 34°C). Just as with the e.p.s.p. depression the presynaptic 

 depolarization is much more effectively produced by the group I afferents 

 from flexor muscles than by those from extensors. Furthermore, they have 

 approximately the same time course: after a latent period of several milli- 

 seconds both reach a maximum at about 15 msec and have a total duration of 

 about 200 msec. 



Investigation into the possible mechanisms of production of the presynaptic 

 depolarization has revealed that the conditioning afferent volleys produce a 

 large field potential in the spinal cord (Fig. 7j). This potential is likewise, 

 produced most effectively by the lb afferent impulses from flexor muscles 

 and it has a time course comparable with the presynaptic depolarization. 

 Since the field is produced by sources at the region of the intermediate nucleus 

 and sinks ventral thereto in the region of the motoneuronal nuclei, a possible 

 explanation is that it is due to the after-hyperpolarization following impulse 

 discharge by the A and B interneurons. particularly the latter (cf. Eccles, 

 Eccles and Lundberg, 1960). 



Thus group I afferent volleys from muscle give rise to four events in the 

 spinal cord, which presumably are related because they have such significant 

 features in common: depression of the e.p.s.p. produced by la afferent 

 impulses, presynaptic depolarization of la afferent fibres, dorsal root reflexes 

 in la afferent fibres, and finally the field potential. For example these events 

 are all produced most effectively by lb afferent impulses from flexors, but also 

 by la impulses and by group I impulses from extensors. Again the latency of 

 all is several milliseconds, and with all but the dorsal root reflex the maximum 

 is at about 15 msec and the duration about 200 msec. Presumably the presyn- 

 aptic depolarization causes the dorsal root reflex in the group Ta afferent 

 fibres, and accommodation accounts for the much briefer duration of the 

 dorsal root reflex. 



Since group lb primary afferent fibres apparently do not penetrate as far as 

 the ventral horn (Eccles, Fatt, Landgren and Winsbury, 1954; Eccles, Eccles 

 and Lundberg, 1957), it may be assumed that the presynaptic depolarization 



