44 Innervation of the Glandular Elements 



glands (Macintosh, 1937; Riker and Wescoe, 1949; Koelle, 1950; 

 Dirnhuber and Evans, 1954; Dumont, 1955; Stromblad, 1955, 

 1956a, 1957a; Kahlson and Renvall, 1956). Histochemical obser- 

 vations show true cholinesterase to be present in a line network of 

 nerve fibres around the acini (Snell and Garrett, 1956, 1957). Ex- 

 periments by Dirnhuber and Evans (1954) suggest that the true 

 cholinesterase plays a more important role for the transmission 

 process than pseudocholinesterase. Using inhibitors acting selec- 

 tively on the true, or on the pseudocholinesterase, they found that 

 the secretory process was particularly influenced by inhibition of 

 the true esterase. Section of the parasympathetic fibres causes a 

 decrease in the esterase activity of the glands; as with acetyl- 

 choline, there is not a complete loss of activity, even after post- 

 ganglionic denervation, but a reduction by about 60 per cent 

 (Stromblad, 1955, 1957a). 



It is well established that parasympathetic stimulation releases 

 acetylcholine from the submaxillary gland of cats and dogs (Babkin, 

 Alley and Stavraky, 1932; Babkin, Gibbs and Wolff, 1932; Beznak, 

 1932; Gibbs and Szeloczey, 1932; Feldberg, 1933; Henderson and 

 Roepke, 1933a and b). The liberation takes place even in the 

 presence of atropine. 



The acetylcholine set free has generally been assumed to originate 

 from the terminals of the postganglionic neurone. In the sub- 

 maxillary gland, however, most of the synapses between the pre- 

 and postganglionic neurone are situated close to the gland or within 

 it, and these synapses are unavoidably included in a perfusion ex- 

 periment. In experiments on submaxillary glands perfused with 

 eserinized plasma, acetylcholine was found to appear in the venous 

 effluent on stimulation of the chorda (preganglionic, parasym- 

 pathetic fibres). Stimulation of the postganglionic neurone, and 

 a consequent release of acetylcholine from its endings, was then 

 prevented by the addition of curarine to the perfusion fluid. When 

 the chorda was again stimulated acetylcholine was still found in the 

 perfusate, but the quantity was reduced to one-quarter to one-third 

 of that found in the absence of curarine. It was concluded that 

 when the plasma contained curarine, the acetylcholine obtained on 

 chorda stimulation originated only from the preganglionic endings, 

 whereas in the absence of curarine the acetylcholine had been 

 liberated both from pre- and postganglionic endings (Emmelin and 

 Muren, 1950). Fig. 3.2 shows two experiments of this kind, one in 



