3- 



o 



10 



20 



30 



seconcs 



Fig. 21. Inhibition of spontaneous ganglion activity, diflferential effect on ganglion 

 burst and heart contraction (Homarus). Large (#) and small ( j filled circles plot 

 burst frequency; large filled O) and open (O) circles plot heartbeat frequency. 

 The large filled circles (#) represent points where burst and heartbeat frequencies 

 coincide. During dorsal nerve stimulation not all bursts produced heart contrac- 

 tions and consequently burst frequency (■) and heartbeat frequency (O) diverged. 

 Stimulation at 49/sec began at on and stopped at ojf. The inhibitor fiber and one 

 accelerator fiber responded to the stimulus. 



(see Fig. 17) and an uncritical evaluation would suggest that inhibition 

 requires several seconds for facilitation and that adaptation is minimal. 

 The actual facts, of course, are directly opposite: adaptation and gradual 

 increase in mean excitability of a critical unit lead to complete inhibition of 

 the heartbeat. 



A similar condition obtains in another experiment in which the normal 

 pacemaker is replaced by a direct stimulus to the ganglion, and brief trains 

 of inhibition are applied immediately before each burst (Fig. 23). The pattern 

 changes of the large spike complex showing "skipped" bursts and hyper- 

 excitability in bursts f to i recall the responses of Unit 2 above and parallel 

 the behavior of the uninhibited ganglion when driven by electrical stimuli 

 at a frequency just beyond the maximum following frequency. In this instance, 

 however, with interrupted inhibitor trains, several bursts are required to 

 reach the fullest inhibition so skipped bursts and super-normal excitability 

 appear only during the latter portion of the series. 



Figure 23 also demonstrates a long-lasting facilitation between inhibitory 

 trains spaced at one second intervals. Terzuolo and Bullock (1958) record 

 similar phenomena in that i.p.s.p. facilitation is more rapid in a second train 



