72 



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J. C. ECCLES 



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Fig. 1. A-F. Lower records give intracellular responses (i.p.s.p.'s) of a biceps- 

 semitendinosus motoneuron to a quadriceps volley of progressively increasing 

 size, as shown by the upper records, which are recorded from the Le dorsal root 

 by a surface electrode, downward deflections signalling negativity. All records 

 are formed by the superposition of about forty faint traces, g shows i.p.s.p.'s 

 similarly generated in another biceps-semitendinosus motoneuron, the mono- 

 synaptic e. p. s. p. 's of this motoneuron being seen in h. i-l show changes in potential 

 produced by an applied rectangular pulse of 12 ■: 10"^ A in the depolarizing and 

 hyperpolarizing directions, i and k. being intracellular and j and l extracellular 

 (Curtis and Eccles, 1959). Reproduced by permission from the Journal of Physiology. 



In Fig. 2a the current flow responsible for the i.p.s.p. has been calculated by 

 assuming that the eff'ective surface of the dendrites is 2-3 times that of the 

 soma, a ratio that was derived from measurements on motoneurons of the 

 lumbosacral cord of the cat (Coombs et al., 1955a). On the basis of measure- 

 ments of a heterogenous series of motoneuronal pictures pubhshed by various 

 authors Rail (1959) argues for a much larger ratio (10-25 or even higher), 

 and consequently for a much longer time constant for the membrane. How- 

 ever, Aitken and Bridger (1961) have measured the somas and dendrites of an 

 extensive series of motoneurons in the lumbosacral region of the cat cord and 

 give measurements both of the relative sizes of the dendrites and soma and of 

 the numbers of dendrites that are in close agreement with the values originally 

 derived for such motoneurons by Coombs et al. (1955a) and employed by 

 Coombs et al. (1959); hence we may assume that in accordance with Curtis 

 and Eccles (1959) the time course of the inhibitory current is approximately 

 given by the broken Hne of Fig. 2a. It will be seen that the inhibitory current 

 virtually ceases to flow just after the summit of the i.p.s.p., the decaying phase 

 being due to the passive recovery of the membrane potential. 



