DIFFERENTIAL GROWTH 167 



cross sections through an experimental and adjacent control nerve at 

 the indicated levels, located one centrally and the other distally to the 

 bottleneck. A detailed analysis of this phenomenon in a large series of 

 varied experiments has led consistently to the same conclusion, namely, 

 that new axoplasm is constantly produced in the nucleated part of the 

 cell body and that the whole column of axoplasm is in steady slow mo- 

 tion in proximo-distal direction. If this translatory movement is par- 

 tially throttled by constriction, the supply to more peripheral levels is 

 correspondingly reduced, while the surplus piles up at the entrance to 

 the narrows. If the constriction is later removed, the effect is much as 

 that of opening flood gates; that is, the dammed up material moves 

 downward, its front advancing, according to preliminary determina- 

 tions, at the order of one millimeter per day. 



There is evidence that this proximo-distal growth of the axoplasm 

 occurs not only during regeneration, when it adds directly to the width 

 of the fiber, but actually goes on continuously in all axons, even the 

 mature ones, which have reached stationary size. The central cell body 

 seems to turn out a steady supply of new axoplasm, most of which is 

 then conveyed distad. This raises the puzzling question as to where the 

 material goes, if it no longer adds to the size of the fiber. I submit that 

 it simply serves to replace the protein systems of the cell as they wear 

 off in a steady natural degradation process, and that the nucleated cell 

 body is, in fact, the sole source of such replacement. We know that any 

 isolated fragment of nerve can exhibit the synthetic phases of respira- 

 tory metabolism with the aid of the enzyme systems it contains. 

 But in the light of our experiments, it would seem that the enzyme sys- 

 tems themselves cannot be synthesized anywhere except in the central 

 cell body, whence they are then distributed over the whole neuron. 



As supporting evidence for this view we can quote the intensive pro- 

 duction of nucleoproteins at the nucleus of the nerve cell (20), the iden- 

 tification of nucleoproteins in the axis cylinder (2), and finally what 

 might be taken to be the external sign of their peripheral breakdown, 

 namely the liberation of nitrogen in the form of ammonia from periph- 

 eral nerve (15). As a matter of fact, a preliminary estimate of the rate 

 of protein breakdown from the known values of ammonia production 

 leads to a figure which is satisfactorily close to the rate of proximo- 

 distal replacement determined from the damming-and-release experi- 

 ments reported above. While details of this concept remain to be worked 

 out, it leaves no doubt that the site of growth and replacement of the 



