14 INVERTEBRATE PHYSIOLOGY 



second or two toward a very constant firing threshold. The burst fre- 

 quency depends then not only on the rate of rise of the generator potential 

 in the fastest pacemaker unit but also on the degree of depression at the 

 end of the last burst, which in turn depended on the activity of many units 

 which participated in the burst, thus on the burst duration and intensity. 

 We are in the presence here of reverberating circuits, but they serve not 

 to maintain activity in a continual self-re-excitation but to "provide means 

 of spontaneously active units to undergo a slower alternating auto-excita- 

 tion and depression" (Maynard). The system is capable of relative sta- 

 bility in the sense that removal or silence or hyperactivity of any or even 

 several units does not greatly upset the pattern. 



These are the observed properties and the inferred mechanisms. I must 

 emphasize that we do not know the connections in detail, and it is still only 

 the simplest inference that these properties are to be explained in terms 

 of the properties of units as recorded from single cells in this ganglion. 

 There is reason to believe that this arrangement is not Hmited to a ganglion 

 with such a small number of cells but applies also to the large, many-celled 

 ganglion of the heart of Limulus. 



Superimposed upon or perhaps underlying the excitatory state which 

 plays the role just described is a sensitivity to physiological degrees of 

 stretch or inflation. We do not know whether this inheres in all the cardiac 

 ganglion cells or only in some, but it appears to be a direct response of 

 these cells and not due to influx from some separate sensory neurons. The 

 effect of stretch is to accelerate or enhance spontaneity. 



In addition to integrating stretch, its own spontaneity, and intramural 

 excitation and possibly inhibition, the cardiac ganglion neurons must also 

 integrate input they receive from two pairs of extramural acceleratory and 

 one pair of inhibitory nerve fibers from the central nervous system, each 

 of whose effects is differential with respect to different aspects of activity 

 and not simply reciprocal with the other. For example, burst frequency 

 and number of spikes per burst are decreased by inhibitory stimulation but 

 spike frequency within a burst may go up. The time courses of develop- 

 ment, adaptation, and after-effects are slower for acceleration and are not 

 mirror images of those in inhibition. 



We do not understand the factors that determine these effects ; at times 

 a change in the tonic level of extramural acceleration or inhibition will 

 change the burst pattern progressively and nearly proportionally for each 

 parameter, at other times it will affect the large followers primarily and 

 may stop output to the muscle without gross change in burst pattern, and 

 at still other times the small pacers are affected more, causing a slowing, 

 for example, of the burst frequency without corresponding depression of 

 the followers, which now escape and fire just before each burst. 



