NEURONAL INTEGRATIVE MECHANISMS 



13 



by positive feedback, and so intensify synaptic excitation as to bring on a 

 compensatory depression terminating the burst. The silent period and 

 hence burst frequency is thus determined not by any single cell but by the 

 integrated activity of several, i.e., by the duration and intensity of the 

 whole burst. The excitability cycle by itself may be sufficient to account 

 for the intermittent activity patterned out of an apparent natural tendency 

 to continuous activity, at least whenever we have several interacting units. 

 When intermittent trains occur in single isolated neurons we must invoke 

 a new underlying oscillatory process, but such instances do not appear to 

 be a normal part of the activity in this ganglion. 



A A fS^ 



Fig. 5. Possible connections of cardiac ganglion leading to patterned burst forma- 

 tion. A. Multiple chain. Top cell is the pacemaker, middle row interneurons, bottom 

 row, motor neurons as proposed by Rijiant for Limulus. B. Closed chain. There is no 

 morphological pacemaker. Every cell acts as motor neuron and at times as pace- 

 maker and as interneuron. Burst formation depends on the properties of interaction 

 rather than on connections. C. Modified closed chain as in lobsters. Small cell acts as 

 pacemaker, but there is feedback, and patterning of burst depends primarily upon the 

 properties of this interaction and its sequelae in the cells. (After Maynard.) 



The system just outlined is a "closed chain" in Maynard's terminology 

 if all cells are equally effective upon each other. The actual observations 

 are most easily understood by considering the cardiac ganglion to be a 

 "modified closed chain" (Fig. 5) with some asymmetrical connections and 

 specialization of function but in which recriprocal interaction and spon- 

 taneity of all units are dominant features. The largest cells are in all likeli- 

 hood incapable of triggering a normal burst of the ganglion, although they 

 are spontaneously active and in special circumstances do pace each other. 

 Their unique role is that of motoneurons, but they act also as integrative 

 neurons which formulate an output that is a function of, but quite unlike, 

 their input, and help to determine burst durations and hence frequency. 



One advantage of this system is its lack of dependence on any one critical 

 value. No one cell fires at the burst frequency, i.e., heartbeat frequency. 

 The pacemaker fires a train in each burst and is simply the first of probably 

 four duplicates. Each of these four, having been turned off at the end of a 

 burst by accumulating hyperpolarization from internal and external 

 sources, develops a slow generator potential rising a few millivolts in a 



