^12 Comparative Animal Physiology 



abolished by atropine.'^^' Calcium is apparently necessary for ACh liberation.«o 

 Curare permits continued liberation of ACh at the motor nerve endings but 

 prevents its depolarizing action, presumably by combining with the chemical 

 receptor substances at the end-plate."^ Depolarization by ACh, nicotine, and 

 caffeine, but not by potassium, can be antagonized by curare. The trans- 

 mission in vertebrate muscle can be summarized as follows: 



curare 



I 

 motor ner\'e impulse >- junctional transmitter >- 



(acetylcholine liberation) 

 end-plate potential >- muscle impulse )- all-or-none-twitch 



i 



local contraction 



An alternative theory^"- '^^- ^^■^- ^"•''" is that acetylcholine is concerned in 

 electrical propagation, that the nerve action potential is the junctional trans- 

 mitter, and that the acetylcholine obtained in perfusion comes from the sole 

 plate of the muscle rather than from the nerve endings. This theory is sup- 

 ported by the distance from nerve ending to sole plate (Fig. 235), by the 

 low permeability of the muscle fiber to acetylcholine except at the region 

 of the end-plate, and by evidence that acetylcholine is concerned in nerve 

 conduction (Ch. 23). Many of these facts can be accounted for by the elec- 

 trical theory as well as by the chemical transmitter theory. Whatever its 

 origin in perfusion experiments, there is little doubt that ACh is an important 

 component in the transmission mechanism. 



Many vertebrate smooth muscles are innervated by adrenergic postgan- 

 glionic sympathetic fibers. Adrenalin (or adrenin) causes responses similar 

 to those produced by sympathetic stimulation. The adrenin-like mediator 

 can be identified in the blood, coming from a region of sympathetic dis- 

 charge.*'^ The action both of the mediator and of adrenalin is antagonized 

 by ergotoxin. The mediator liberated in structures which are inhibited by 

 the sympathetics differs quantitatively in its effects on test muscles from that 

 liberated in structures which are excited, and the inhibitory agent may be 

 adrenin, the excitatory agent nor-adrenin.^^ There is good evidence that the 

 nerves eliciting contraction of pupil constrictors are cholinergic. 



The evidence regarding chemical mediation at motor nerve endings in 

 invertebrate animals is inadequate. Acetylcholine liberation in muscle is es- 

 tablished only for annelids and sipunculoids, is indicated in molluscs and 

 echinoderms, and is unlikely in arthropods and coelenterates.^'^ 



The most convincing evidence for cholinergic motor nerves is found among 

 annelid and sipunculoid worms. The muscles of many worms of these groups 

 contain ACh and ChE (Table 73). The body wall muscle is stimulated to 

 contract by acetylcholine, and sensitivity is increased by eserine. Sensitivity 

 is great (10~"), even without eserine, and body wall muscles of the leeches 

 Hiriido and PontohdeUa have been used in bioassay. The action of ACh 

 antagonists should be investigated further. It has been reported that nerve 

 activation is paralyzed by curare in Hirudo (but not in Lumbriciis'), by B- 

 erythroidine in Lumhricus, and by atropine in Sipimculus and Aphrodite. 

 Nicotine abolishes the direct effect of ACh on the earthworm body wall.-'^'-' 



