162 DONALD M. MAYNARD 



position must await conductance measurements across the neuron membranes 

 during inhibition. 



One important question regarding inhibitory ''excitation" now seems to 

 be whether the membrane potential of certain neurons in the in situ ganghon 

 may normally lie above the reversal potential for i.p.s.p.'s. AUhough some 

 of the units having depolarizing i.p.s.p.'s give reasonably normal discharges 

 during a burst (Fig. 14) others are obviously abnormal (Fig. 15). They 

 produce no propagated spikes and are activated by a single presynaptic 

 unit. 



Rebound Effects 



Unlike the phenomena of inhibition and adaptation, post-inhibitory re- 

 bound is not reflected in underlying membrane potential shifts. Indeed, post- 

 inhibitory spikes may rise from a soma membrane potential several millivolts 

 higher than that found before inhibition (Fig. 16). The rebound appears 

 associated with some process leading to more rapidly developing generator 

 potentials (Fig. 14) and is obvious only when the i.p.s.p.'s hyperpolarize or 

 stabihze the membrane. There is some support, therefore, for the contention 

 that post-inhibitory rebound may be compared with the rebound following 

 release of hyperpolarizing currents or electrotonic depression (Hagiwara and 

 BuUock, 1957). 



The results of intracellular recording are generally compatible with the 

 idea that the major effect of activity in the inhibitor fiber is to alter membrane 

 permeabihty to some specific ion, by analogy with other systems, K+ or Cb. 

 Two observations, however, do not seem to fit directly into the hypothesis. 

 First, biphasic i.p.s.p.'s occur (see also, Tauc, 1958); second, the reversal 

 potential of the summed i.p.s.p.'s may not necessarily be that of the individual 

 i.p.s.p. (Otani and Bullock, 1959). Although it is possible to invoke anatomical 

 distributions of the inhibitor terminals to account for these observations, 

 such an explanation will not be completely acceptable until careful con- 

 ductance measurements have been made during inhibition. 



One criticism has been raised by Dr. C. A. G. Wiersma regarding the 

 interpretation of the above results, i.e. there is no conclusive evidence that 

 unknown accelerator fibers are not being stimulated with the inhibitor and 

 are responsible for such things as the biphasic i.p.s.p.'s This is indeed an 

 important point, particularly when stimulation of the inhibitor is achieved 

 in the dorsal nerve as in at least some preparations of Terzuolo and Bullock 

 (1958) and Otani and Bullock (1959). Although the criticism cannot be 

 completely answered at present, I do feel that the physiological and anatomical 

 evidence presented earlier, and the sharp thresholds for the effects reported 

 by Terzuolo and Bullock (1958) make additional accelerator activity unhkely, 

 at least when the inhibitor fiber is stimulated in segmental nerve 1. 



