Nervous System 



383 



fail to evoke a corresponding cellular in- 

 crease in the spinal limb centers (Schwind, 

 '31; Harrison, '35a). On the other hand, 

 genetically hyperdactylous mice have been 

 reported to have larger limb cord segments 

 (Tsang, '39; Baumann and Landauer, '43). 

 Whether this increase of central cell number 

 as a result of the presence of extra toes is 

 as limited as that observed in urodeles or 

 whether the limb centers of rodents have 

 perhaps retained a higher output capacity 

 from their phylogenetic past, when they pos- 

 sessed more toes, is an open question. 



Rebound on Secondary Units. Modifications 

 of the size of spinal ganglia due to altera- 

 tions of the periphery are also reflected in 

 corresponding variations of the sensory col- 

 umns of the spinal cord with which the 

 former connect (Hamburger, '34; Barron, 

 '45). This demonstrates the existence of 

 transneuronal effects "in series" similar to 

 the transneuronal effects "in parallel" just 

 discussed. Instead of a non-neural periphery 

 affecting its correlated neurons, one neu- 

 ronal group now influences the quantitative 

 development of another to which it bears an 

 effector relation. No numerical increase of 

 the internuncial cells discharging into the 

 motor columns has as yet been seen to 

 follow an induced increase of the latter, 

 although the reverse, secondary degenera- 

 tion of more proximal neurons in conse- 

 quence of destruction of central fiber tracts, 

 has been observed (see Bodian, '42). 



Results comparable to those in the spinal 

 segments have also been obtained with 

 cranial nerves. Elimination of the labyrinth 

 including the acoustic ganglion entails 

 underdevelopment of some associated cell 

 groups of the medulla (Levi-Montalcini, 

 '49). After the early removal of one eye 

 in larval amphibians, the midbrain roof 

 of the opposite side, end station of the 

 crossed optic nerve fibers, develops defec- 

 tively. Its size remains subnormal (Steinitz, 

 '06; Diirken, '13; Larsell, '31), mitotic ac- 

 tivity being reduced and the segregation 

 of typical cell strata being impaired (Koll- 

 ros, '53). As in the spinal centers, the effect 

 is complex in nature, involving proliferation, 

 migration and cell enlargement, although in 

 the present case it is transmitted not directly 

 but through intermediary neurons. 



It is not surprising to find that the mor- 

 phological underdevelopment of an eyeless 

 midbrain hemisphere is reflected in a deficit 

 of its chemical products. Thus, the activity 

 of acetylcholinesterase, an obligatory con- 

 stituent of neural tissue, is reduced in pro- 



portion to the reduced number of nerve 

 cells (Boell and Shen, '51). 



Midbrain centers connected with eyes of 

 subnormal size (transplantation from small 

 to large animals) are intermediate between 

 those of normal and anophthalmic specimens 

 (Twitty, '32). Genetically determined re- 

 duction or suppression of eye development 

 (microphthalmia, anophthalmia) has the 

 same effect on the size of the optic brain 

 centers as has the corresponding experi- 

 mental interference (Chase, '45). It is note- 

 worthy that in insects, too, eye reduction, 

 either experimentally produced (Kopec, '22) 

 or genetically caused (Power, '43), is cor- 

 related with reduction of optic ganglia. 

 Cephalopods react similarly (Ranzi, '28). 



An artificial increase in the volume of 

 optic nerve fibers reaching the brain yields 

 the expected central enlargement. This has 

 been obtained in the midbrain after replace- 

 ment of the normal eye by one of excessive 

 size (Harrison, '29; Twitty, '32), or after 

 adding a supernumerary eye (Pasquini, '27) ; 

 and in the medulla, in response to the entry 

 of an aberrant optic nerve from an eye 

 grafted in the place of an ear (May and 

 Detwiler, '25). 



In conclusion, there is widespread evi- 

 dence of quantitative regulation of the 

 maturation of nerve centers from both the 

 effector and receptor ends. Although the 

 modes of action may differ, the principle is 

 the same whether the "receptors" and "ef- 

 fectors" concerned are sensory organs and 

 muscles or other neuron groups. Presumably 

 some of the intracentral regulations out- 

 lined below (p. 386) are manifestations of 

 this same principle. Its operation provides 

 the nerve centers with the necessary latitude 

 of adjustment to insure adequate central 

 control despite the wide individual variabil- 

 ity and unpredictability of the detailed pat- 

 terns of innervation illustrated throughout 

 this article. It is important, however, to 

 remember that the degree of adaptive lati- 

 tude is limited by intrinsic properties of the 

 responding centers which date back to their 

 earlier prefunctional and even preneural 

 stages. 



Specific Modulation and Resonance. The pe- 

 ripheral encroachment upon central develop- 

 ment reaches its climax of refinement in the 

 process of qualitative adaptation ("modula- 

 tion") of neurons in conformance with the 

 type of effector or receptor organ with which 

 they connect. Let us explain this phenome- 

 non in the case of muscle innervation where 

 it was first discovered (Weiss, '24). 



