PERIPHERAL AUTONOMIC MECHANISMS 



995 



fibers. There is no conclusive evidence for the view 

 adopted, for instance by Rosenblueth (292, 366, 367), 

 that the autonomic C axons in general degenerate 

 considerably more slowly than large somatic fibers, 

 which usually show conduction failure 2 to 4 days 

 after transection (80, 135, 292, 366). The slowest 

 known autonomic C fibers lose the al:)ility to conduct 

 impulses within 5 days, as shown by direct recording 

 (310). 



In the course of the Wallerian degeneration of pre- 

 ganglionic fibers, synaptic transmission fails at a 

 stage when impulse conduction mav be largely un- 

 impaired (90). Usually transmission declines rapidly 

 between 24 and 48 hours after nerve section, to dis- 

 appear within 72 hours (13, 97, 90, 206). This is in 

 good agreement with the time range reported for the 

 transmission failure in voluntary muscle (292, 367, 

 407). Rosenblueth has concluded (cf. 362) that 

 synaptic failure is not due to an early degeneration of 

 the nerve endings, as suggested Ijy Titeca (411), but 

 to a decrease of the acetylcholine liberated by the 

 nerve impulses. There is good evidence that acetyl- 

 choline is concentrated in the ner\e endings and that 

 it disappears, and the endings lose to a high degree 

 the ability to synthesize acetylcholine after pregan- 

 glionic transection at the same time as the transmission 

 fails (13, 142, 302, 303). Furthermore, as both the 

 structural and functional degeneration seem to have 

 a progressive centrifugal course (80, 292, 366), the 

 conclusion seems to be justified. It may be questioned, 

 however, whether the demonstration of progressive 

 degeneration in the nerve trunk is conclusive evidence 

 against the occurrence of an early degeneration of the 

 nerve endings. Axon terminals in the motor end plate, 

 for instance, seem to disintegrate earlier than the 

 supplying fibers (206). This may be the case also for 

 the terminal intraganglionic fibers (103). 



Slight changes in the Nissl substance and some cell 

 shrinkage have been reported to occur with pre- 

 ganglionic degeneration (189, 282, 328, 397), but this 

 has been questioned (374). Apart from supersensi- 

 tivity, chronically denervated ganglia show altered 

 reactions to ganglion-blocking agents, suggested to be 

 due to a fall in the intracellular potassium content 



(338, 339)- 



The retrograde reaction in autonomic ganglia 

 initiated by section of the postganglionic nerves pro- 

 duces cytological changes similar to those seen in 

 somatic neurons and recently the similarity has been 

 found to extend to the functional changes (i, 2, 55). 

 After axotomy of the postganglionic neurons, impulse 

 transmission in the ganglia is rapidly impaired and 



almost completely abolished within 2 weeks. Later 

 there is a slow recovery stage. Many of the cells 

 have become irre\ersibly changed, however, as both 

 the transmitted response and the spike potential 

 obtained by direct stimulation of the postganglionic 

 nerve are markedly reduced. The transmission failure 

 seems to be due to changes in the soma of the post- 

 ganglionic cells resulting in a lo.ss of sensitivity to 

 liberated transmitter. 



Regeneration 



The data hitherto reported concerning the various 

 aspects of regeneration in the autonomic nervous 

 system are incomplete, unsystematic and often highly 

 contradictory. It is not therefore possible to treat this 

 subject more than purelv superficiallv. Regeneration 

 in the peripheral nervous system has recently been 

 reviewed {185). 



Whether regeneration of autonomic nerve fibers 

 differs fundamentally from that of somatic fiijers has 

 not been adequately studied. That such differences 

 may exist in the case of nonmeduUated fibers is sug- 

 gested by the report of Nageotte (325) that their 

 sheaths form a syncytial network. NonmeduUated 

 fibers often are composed of a sheath enclosing several 

 fibers (162, 204, 325). Again, the Schwann cells of 

 autonomic nonmeduUated fibers do not multiply 

 after nerve section (235, 236, 416). Nevertheless, such 

 studies as have been made of regeneration of auto- 

 nomic fibers have failed to reveal obvious differences 

 from that of somatic fibers (97, 98, 279, 282). 



From data obtained by indirect methods (56, 57, 

 285, 286, 334, 413) the rate of growth in the cervical 

 sympathetic trunk of the cat, rabbit and dog may be 

 estimated to be i to 2 mm per day if scar and matura- 

 tion delay are taken into account. This is in good 

 agreement with values found in a more systematic 

 study of cat and rabbit (67) where the rate of advance 

 of functional recovery after crushing the cervical 

 sympathetic trunk was estimated to be 2 mm per day 

 for the cat and to i .6 mm per day for the rabbit. The 

 functional return, as determined by the disappearance 

 of paralysis after section or crushing of the cervical 

 sympathetic trunk in the cat, has been reported to 

 occur within 2 to 6 weeks depending on the site of 

 lesion (56, 57, 67, 286, 389). In some animal species 

 (especially the cat) the preganglionic fibers have a 

 high capacity for bridging even very large gaps (67, 

 206, 239-241, 286); in other species (the rabbit for 

 instance) this capacity is, on the contrary, very re- 

 stricted (67). It is possible that the differences are 



