no Effects of Denervation 



in the nictitating membrane, and an intact sympathetic trunk does 

 not at all counteract the development of the chorda supersensi- 

 tivity. The nictitating membrane is constantly activated via the 

 sympathetic fibres; the salivary glands, on the other hand, are 

 activated mainly via the parasympathetic fibres. If, however, the 

 traffic of impulses for the gland via the sympathetic is greatly in- 

 creased by reinnervating the gland from the hypoglossal nerve via 

 the sympathetic fibres the chorda supersensitivity is found to de- 

 crease (Emmelin, Muren and Stromblad, 19576). All these obser- 

 vations seem to be compatible with the concept that supersensitivity 

 is a consequence of lack of secretory impulses, from the central 

 nervous system under ordinary conditions, or via the blood in 

 the experiment when secretory agents are injected. 



Such a hypothesis cannot, however, provide the whole explana- 

 tion. It does not account for the fact that section of postganglionic 

 parasympathetic neurones, or treatment with suitable parasym- 

 patholytic drugs, causes a higher supersensitivity than does section 

 of the preganglionic parasympathetic fibres or treatment with a 

 ganglionic blocking agent. Nor does it explain the fact that excision 

 of the superior cervical ganglion, but not preganglionic sympathetic 

 denervation, produces a supersensitivity — a supersensitivity that 

 can be superimposed upon that produced by section of the pre- 

 ganglionic, or even postganglionic parasympathetic fibres. In 

 order to account for these facts it seems necessary to assume that 

 there is a continuous release of the transmitter from the postgan- 

 glionic endings, as discussed on page 63 ; and that this leakage, 

 although it causes no secretion, is able to counteract, to some 

 extent, the development of supersensitivity (see Emmelin, 19606). 



Hence, preganglionic denervation, or treatment with a ganglionic 

 blocking compound, should cause a supersensitivity because the 

 gland is deprived of transmitter, released by the nerve impulse. 

 Postganglionic denervation, or treatment with a parasympatholytic 

 agent, should cause a greater supersensitivity because in addition 

 no leaking transmitter acts on the gland cells. In the sympathetic 

 system this latter factor may be the main one; removal of the 

 superior cervical ganglion therefore causes a moderate super- 

 sensitivity only. 



It seems reasonable to assume that the process of sensitization 

 is related to some part of the receptor region rather than to the 

 secretory mechanism. The continuous influence of the postgan- 



