THE SYNAPTIC MECHANISM FOR 

 POSTSYNAPTIC INHIBITION 



J. C. ECCLES 



Department of Physiology, The Austrahan National University, Canberra, A.C.T. 



It will be convenient if I restrict my account almost entirely to the simplest 

 type of postsynaptic inhibition in the nervous system, namely the inhibitory 

 action of group la afferent impulses on motoneurons. There is much evidence 

 that all other types of postsynaptic inhibition have essentially the same syn- 

 aptic mechanism, both as regards transmitter substance and ionic perme- 

 ability (Eccles et al., 1954; Coombs et al., 1955a; Eccles, 1957; Curtis, 1959). 

 The differences in time course are attributable either to temporal dispersion 

 or to repetitive discharge of the inhibitory presynaptic impulses. 



Intracellular recording reveals that inhibitory synaptic action by a la 

 afferent volley causes a brief hypcrpolarization of the motoneuronal mem- 

 brane (Fig. 1a-f). The microelectrode must be filled with a salt having a large 

 anion such as sulphate or citrate, else this inhibitory postsynaptic potential 

 (i.p.s.p.) is likely to be distorted by intracellular changes in ionic composition, 

 as will be seen later. Variations in the size of the group la afferent volley 

 cause alterations in the size of the i.p.s.p., but not in its time course, which 

 has characteristically a brief rising phase and a slower, approximately expo- 

 nential, decay; hence it can be assumed that the i.p.s.p. is produced by a 

 virtually synchronous action of inhibitory impulses, and that each impulse 

 produces an i.p.s.p. having the same time course as those illustrated in Fig. 

 1a-f for afferent volleys of varying size. 



When one comes to consider in detail the synaptic events responsible for 

 the hyperpolarization of the i.p.s.p., it is evident that the increased charge 

 on the motoneuronal membrane must be caused by ?n electric current out- 

 wardly directed across the subsynaptic membrane of the activated inhibitory 

 synapses and inwardly directed across the remainder of the membrane, so 

 hyperpolarizing it, as illustrated in Fig. 2b, d. The time course of this current 

 can be approximately calculated if the electric time constant of the moto- 

 neuronal membrane is known (Curtis and Eccles, 1959). This time constant 

 is not directly given by the time course of the membrane potential change 

 produced by application of a rectangular current pulse through an intra- 

 cellular electrode (Fig. 1, i, k). A considerable allowance has to be made for 

 the distortion produced by electrotonic spread of current along the dendrites. 



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