52 J. C. ECCLES 



cord of the inhibitory and excitatory volleys has been diminished progres- 

 sively from 0-85 to 0-28 msec and correspondingly the deviation point has 

 occurred progressively later on the reflex spike. When, as in Fig. 3a-f, the 

 inhibitory volley is at a fixed position (the first vertical broken line) the devia- 

 tion points lie close to a second vertical line, which is in this figure 1-58 msec 

 later. This interval gives the central latency for inhibitory action on reflex 

 spike discharge if a small aUowance (in this case 0-28 msec) is made for impulse 

 conduction time from its origin in the initial segment of the motoneuron to the 

 recording point on the ventral root (h), i.e. the central inhibitory latency is 

 1-31 msec. This value is in good agreement with the latency of the i.p.s.p. 

 (1-37 msec) intracellularly recorded from one of the motoneurons that 

 contributed to the reflex spike (g). In a series of six experiments of this type 

 the latency of the i.p.s.p. was sampled in twenty-four motoneurons and was 

 always within 0-1 msec of the central latency for inhibition of the reflex spike 

 discharge. 



Similarly, in all of the many series in five experiments with the contralateral 

 inhibition at S3 level, there was excellent agreement (within 0- 1 msec) between 

 the latencies of the intraceflular i.p.s.p. 's and of the inhibitory action on reflex 

 spike discharges. Thus the experimental evidence refutes the postulate of 

 Lloyd and Wilson (1959) that there is an earlier inhibitory process having no 

 electrical sign, yet causing the inhibition of impulse discharge and somewhat 

 (up to 1 -0 msec) later the i.p.s.p. with its action in inhibiting the spike potentials 

 that are recorded intraceUularly in motoneurons. Incidentafly this postulate 

 also is at variance with the evidence that the IS component of the spike 

 recorded in the motoneuron signals the initiation of the impulse discharged 

 into the ventral root (Coombs et al., 1957). Apparently Lloyd and Wilson 

 have confused the IS with the later SD spike. 



It now remains to summarize in a diagram (Fig. 4) the time course of events 

 when a monosynaptic reflex spike is inhibited by a volley that enters the spinal 

 cord simultaneously, which gives the latest time at which an inhibitory volley 

 can be effective. All the detailed times of the various events are derived from 

 direct measurements. For example, the brief intervals of 0-3 msec (ESD or 

 ISD) between the arrivals of presynaptic impulses at the synaptic terminals 

 and the initiation of an i.p.s.p. or e.p.s.p. are based on the evidence cited above. 

 Furthemiore, the intervals between the onset of the e.p.s.p. and the initiation 

 of spike discharges are also directly observed. The additional delay of about 

 0-8 msec in the central inliibitory pathway is shown in Fig. 4 to be satis- 

 factorily explained by the synaptic relay in the intermediate nucleus. 



As win be argued in another Chapter (Eccles, 1961b), when inhibition is 

 produced by a group la afferent volley, the various inhibitory synapses are 

 activated once only and virtually simultaneously. When the size of the group 

 la volley is varied, there is merely an alteration in the number of activated 

 synapses, and the time courses both of the reflex inhibition and of the i.p.s.p. 



