LOCAL NERVE CENTRES. 673 



accompany the arteries and run past the submaxillary ganglion without 

 entering it. Further, it is easily shown that the sympathetic fibres are 

 connected with nerve cells in the superior cervical ganglion, and that 

 stimulation of the nerve fibres on either side of the ganglion has the 

 same result, namely, contraction of the arteries. 



In the case of the nervus erigens, the facts are of the same nature. 

 Nearly all the sympathetic fibres — which are vaso-constrictor — end in 

 connection with nerve cells in the sacral sympathetic ganglia ; stimula- 

 tion on either side of these ganglia causes great contraction of the 

 vessels of the penis— section on either side of these ganglia causes great 

 vascular paralytic dilatation. The fibres given off by the sacral ganglia 

 have no nerve cells on their course to the periphery, for nicotin 

 does not paralyse them. On Bernard's hypothesis, then, the sacral 

 ganglia would be the local centres which are inhibited by the nervus 

 erigens, but in fact the nervus erigens has no connection whatever with 

 these ganglia. If, then, the nervus erigens inhibit local vaso-constrictor 

 ganglia, there must be some such ganglia in addition to the sacral 

 ganglia, and situated more peripherally. All the evidence, however, 

 goes to show that the ganglia in the course of the nervus erigens are 

 vaso-dilator and not vaso-constrictor. Stimulation peripherally of these 

 ganglia causes vaso-dilatation, and nicotin annuls the effect of stimulat- 

 ing centrally of the ganglia, but does not annul the effect of stimulating 

 peripherally of them. 



Both for the chorda tympani and for the nervus erigens we have, 

 then, satisfactory evidence that the vaso-dilator fibres run to nerve cells, 

 and that both pre-ganglionic and post-ganglionic fibres produce vaso- 

 dilator effects ; further, that the vaso-constrictor fibres run to nerve 

 cells, and that both pre-ganglionic and post-ganglionic fibres produce 

 vaso-constrictor effects ; lastly, that if the two systems communicate, it 

 can only be in the region of the post-ganglionic fibres. 



The state of things is essentially the same in the case of the vaso- 

 dilator fibres of the bucco-facial region of the dog, the inhibitory fibres 

 of the heart, and the inhibitory fibres of the stomach and intestine. 

 And we may conclude for all cases that the inhibition which we are 

 considering is not produced by a lowering of the activity of sympathetic 

 or similar nerve cells. 



We must, look, then, for the mechanism of inhibition either in inter- 

 ference of nervous impulses in the peripheral region of the post- 

 ganglionic fibres, or in a direct action of the inhibitory fibres upon the 

 tissue. 



On the one alternative, constant motor impulses would be annulled, 

 and no longer reach the tissue ; on the other, the tissue itself would be 

 affected, so that such motor impulses as did reach it would not have 

 their usual effect. 



The former is essentially the mode of action suggested by Bernard, 

 but the action takes place in a different part of the nervous apparatus. 

 The peripheral apparatus in which it is conceivable it should take place 

 is either — (a) a nerve cell apparatus, the existence of which we have at 

 present no sufficient reason for believing; or (b) a nervous network, 

 into which both motor and inhibitory fibres run. 



But such a network could not of itself keep up a tonic constrictor 

 action, so that, if inhibition is produced after degenerative section of the 

 constrictor fibres, it can only be produced by a direct action on the tissue. 

 vol. 11. — 43 



