594 ANNALS NEW YORK ACADEMY OF SCIENCES 



parallel fibers, spirals of one on another, multiple contacts, etc., as well 

 as the orthodox small end-foot stuck on a large surface, like a match 

 stick on a cheese; the problem of multiple synapses on a cell body and 

 the relative area of end-feet and their surround; the presence of ir- 

 reciprocal conduction with protoplasmic continuity, as in an asymmet- 

 rically compressed sartorius muscle. Neither these, nor the spatial 

 theory of inhibition, nor the need for regarding the E. E. G. as an oscil- 

 lating somatic potential, problems which have received attention in 

 this publication and elsewhere,^* can be here expanded.) 



The evidence for a transmitter role of ACh in the central nervous 

 system, on the contrary, is inferential and conflicting. Those who 

 have read Feldberg's recent review of this question'^ must have been 

 impressed by the poor case that can be made. Added eserine, or ACh, 

 or both, may increase the activity of a brain region, or depress it, or 

 cause negligible change. The failure of ACh to alter frog cord re- 

 flexes, mentioned by Eccles, is a case in point. Or ACh may excite, 

 while eserine depresses. Atropine, on the whole, does nothing. The 

 two compounds mentioned by Oilman, both powerful anti-esterases and 

 both able to produce convulsions, one of which is completely antidoted 

 by atropine, while the other is uninfluenced by it, afford an instance 

 of the conflicting facts in this area. Strychnine is supposed to exert its 

 action by blocking ChE, yet Tobias^^ has found the ACh content of 

 frog and rat brains and cords decreased, if anything, by strychnine. 

 Nembutal, conversely, increases the ACh content, although, as Bo- 

 dansky mentioned, it also lowers ChE activity. If ACh is an agent 

 for evoking neurone activity, it should increase the oxygen consump- 

 tion of brain. Lipton has recently made Q02 measurements on rat 

 brain slices, at my request, and found no influence of eserine (10"^) alone 

 with eserine and ACh (10"^), at most a better maintenance of the usual 

 initial rate. Incidentally, the only other observations I have found on 

 the influence of ACh on respiration are one"° showing an increase in 

 salivary gland oxygen consumption, and a forgotten one from my own 

 laboratory^^^ showing a marked decrease in the oxygen consumption 

 of nerve (uneserinized). 



The best basis for invoking chemicals in synaptic transmission is 

 that synaptic potentials, like those of the end-plate, may last much 

 longer than could any reasonable physical discharge period for mem- 

 branes with capacitances and resistances in the range known. Then one 

 invokes some active depolarization process, as for nerve; and then this 

 must be explained, by a chemical reaction of some sort. To be sure, 

 chemical activity is involved, as in nerve, and quantitatively more in- 



