HARRY GRUNDFKST I37 



effects in the membrane of adjacent elements which affect their excitabiUty 

 (93, 104, 116, 138, 165). Electrical inexcitability of the postsynaptic membrane 

 therefore would provide a considerable measure of immunity from the perturb- 

 ing influence of electric field effects to the synaptic pathways upon which the 

 precision of integrated nervous functioning depend (99). 



d) Synaptic Transmitters. At least two synaptic transmitters are presently 

 distinguished, acetylcholine and some form of adrenaline-noradrenaline com- 

 plex (30, 78, 146). However, it is not at all unlikely that others also exist. The 

 synaptic transmitters of the mammalian central nervous system in particular 

 do not seem to fit into the two accepted categories. The agents causing the 

 excitatory and inhibitory p.s.p.'s at the motoneuron probably do not belong to 

 either category (64), although it is believed that the transmitter for excitation 

 of the inhibitory (Renshaw) cells is acetylcholine. Neurohumoral activity has 

 been recently demonstrated in the cortex (cf. 120), particularly by the use of 

 cross-perfused preparations (162), but the transmitter nature is unknown. A 

 possible clue to variously discrepant data is provided by the finding (58) that 

 inactivators particularly effective for pseudocholinesterases are better cortical 

 poisons than are those which specifically attack the 'true' (acetyl-) cholines- 

 terase, while the reverse is the case for the muscle end-plate. Thus, structural 

 analogs of acetylcholine, if not the latter, might act as transmitters at the 

 central nervous synapses. Differential sensitivity to various pharmacological 

 agents (161, 163) also indicates that a number of different synaptic mechanisms 

 probably exist. 



The relatively high concentration of cholinesterase present in the eel electric 

 organ, chiefly at the innervated faces of the electroplaques (52), tempts the 

 conclusion that acetylcholine is the synaptic transmitter of this system (cf. 

 100). The fatigability of synaptic transfer in eel electroplaques with a con- 

 committant exhaustion of acetylcholine (42) supports this. The eel electric 

 organ does not, however, respond to injections of acetylcholine (6) whereas 

 that of Torpedo, which is similar in properties to the muscle end-plate (100) 

 does respond electrogenically to the drug (77). 



Proportionality between cholinesterase concentration and the voltage pro- 

 duced by blocks of the eel electric organ have been assumed (150) to support 

 the theory that acetylcholine has electrogenic properties in electrically excit- 

 able, spike generating membrane. This is probably an unjustified conclusion 

 drawn from two types of parallel data, in which the common factor happens to 

 be the excitable surface of the individual cells. The voltage is proportional to 

 the number of these cells in series (4, 14, 130). Also proportional to the number 

 is the area of the innervated, excitable membrane at which cholinesterase is 

 concentrated (52) probably in relation to synaptic, electrically inexcitable 

 membrane. Recent data from Nachmansohn's laboratory (3) also appear to 

 contradict that theory. The resistance of the electroplaque membrane rises 



