170 



DONALD M. MAYNARD 



60 



seconds 



Fig. 24. Post-inhibitory rebound, absence of frequency rebound (Panulirus). 

 ( + ), burst frequency per second; (■), burst duration in seconds; (#), number 

 of large cell discharges per burst. Inhibitor stimulation at 52/sec began at on, 

 continued for approximately 50 sec (note break in abscissa), and stopped at off. 

 Vertical lines give range of values which occurred during break in abscissa. The 

 large cell discharge, which was almost completely inhibited, and to a lesser 

 extent burst duration, rebound following inhibition while the burst frequency 



does not. 



burst, therefore, superficially failed to show post-inhibitory excitation be- 

 cause of inco-ordination of the component units. A record of the heart beat 

 of such a ganglion would likewise show no post-inhibitory excitation even 

 though it was clearly present in the individual ganghon neurons. 



In the second instance (Fig. 24), small units are relatively unaffected by 

 inhibitory activity and show rebound only in increased burst duration. The 

 large units on the other hand, though rebounding in the form of increased 

 number of impulses per burst during post-inhibitory bursts, do not increase 

 the burst frequency. It is fikely that the relative effectiveness of a motor axon 

 impulse in producing myocardial tension declines as it occurs later in a train 

 of such impulses. Consequently, though stronger heartbeats may be expected 

 after inhibition, they need not directly reflect the extent of ganglion cell 

 rebound during a burst. As here and in Fig. 17 slightly stronger heartbeats 

 may be associated with appreciably longer inter-burst intervals, and the 

 general impression is one of post-inhibitory depression rather than the post- 

 inhibitory excitation which actually exists. 



Primary depression of pacemakers rather than followers occasionally 

 occurs, at least in preparations lacking the normal small cell complement. 



