192 Prof. J. N. Langley. On Nerve Endings and on [May 24, 



The difficulty, then, which we have to face is that of reconciling the fact 

 that adrenalin has a special relation to tissues innervated by sympathetic 

 nerves, with the deduction from the degeneration experiments that adrenalin 

 does not act on the nerves or their endings. Elliott, adopting the theory 

 that nerve and unstriated muscle are continuous, considers that adrenalin 

 acts on the junction of the two — the myo-neural junction — and does not act 

 either on muscle or on nerve endings. 



It is important to keep clearly in mind that the question whether 

 adrenalin does or does not act on muscle or on nerve endings is, up to 

 a certain point, a matter of nomenclature. 



If the nerve, the myo-neural junction, and the muscle, are regarded as 

 successive parts of a continuous mass, it may then logically be said, on 

 this theory, that adrenalin acts on the myo-neural junction and does not act 

 on muscle or on nerve. But the conclusion depends upon the definition 

 of muscle and of nerve. The junction, since it is not regarded as a separate 

 entity comparable to the muscle cell or the nerve cell, must consist either 

 of muscle substance or of nerve substance, or of both. That is to say, 

 adrenalin must act either on muscle substance or on nerve substance, or 

 on both. And as muscle substance is a part of the muscle cell, and a nerve 

 substance is a part of the nerve cell, it cannot, from this point of view, be 

 properly asserted either that adrenalin does not act on muscle, or that it 

 does not act on nerve. The legitimate statement from the premises is that 

 it does not act on any muscle substance or on any nerve substance outside 

 the limits of the myoneural junction. 



Two arguments which have been used against the view that adrenalin acts on muscle 

 should, I think, be definitely discarded. Dixon, Brodie and Dixon, and Elliott argue that 

 since, after apocodeine, adrenalin does not stimulate certain unstriated muscle, and 

 barium chloride does, adrenalin cannot act on muscle. This is the traditional argument 

 used with regard to the effect of curarKon nerve endings in striated muscle. It rests on 

 the identification of the contractile molecule of muscle with the whole muscle substance. 

 It is not only conceivable that the irritable substance should be part of the sarcoplasm, 

 but also that it might be a radicle of the contractile molecule. And in either case the 

 irritable substance might be put out of action without destroying the contractile power 

 of the muscle. 



Elliott argues also that it is unlikely that the blood vessels of the lungs or heart should 

 differ in their intrinsic musculature from those of the intestine to such a biochemical 

 degree that the one set should be slightly dilated by adrenalin and the other powerfully 

 contracted. But, in fact, there is variation, and this can only be explained by a variation 

 in nerves or muscles, and the variation might theoretically take place as well in the 

 muscle as in the nerve. 



As regards the localisation of the receptive substance, strong evidence 

 that this occurs to a considerable extent is afforded by the action both 



