364 Dr. W. M. Bayliss. On Reciprocal [Jan. 20, 
normal, not followed by a rise. Accordingly, a further dose of the drug, 
3 milligrammes, was given; this had the effect of completely converting the 
deptessor effect into a considerable rise. At a time, therefore, when the 
constrictor centre is inaccessible to the normal excitations, it can still 
respond to the excitatory action of what were previously inhibitory impulses. 
It appears as if the drug is in some way used up or taken into combination 
in the inhibitory synapse, in order to perform its function of reversal. 
In this connection it is advisable to refer to what may seem a simpler 
explanation of the strychnine reversal than that given by Sherrington. The 
usual account of the action of the drug is that it acts upon synapses so as to 
render those permeable which were previously closed. If we assume that the 
depressor has connections with the constrictor centre which only became 
permeable under the action of the alkaloid, and that these are excitatory im 
nature, the result may be explained. The hypothesis is not in agreement with 
experimental facts. We have seen that the connections with the constrictor 
centre are always open in the normal state, but that their mode of action is 
not excitatory but inhibitory. Moreover, it seems rather that, at all events in 
this particular case, the action of the drug is of the nature of a block. In the 
experiment described above, what was especially noticeable was the long latent 
period of the constriction from the reversed depressor. The rise of pressure 
from the median commenced, at most, two seconds after the beginning of 
excitation, whereas that from the depressor under strychnine, in the first. 
excitation, was 22 seconds; in fact I thought that the second dose had been 
followed by paralysis, so long a time elapsed before any effect was produced. 
The second excitation had a somewhat shorter latent time, viz., 18 seconds. so 
that something of the nature of “ facilitation ” took place. The third excita- 
tion had the same latent time as the second. This fact, on the face of it, looks. 
more like obstruction than the breaking down of barriers. It 1s worth men- 
tioning that this rise of pressure was accompanied by constriction in the limb, 
so that it was a real excitation of the vaso-constrictor centre. 
With respect to the mode of action of the drug, there is one more point 
worth calling attention to. As shown in fig. 15, this is not done by first. 
abolishing the inhibition and then replacing it by excitation, but by pro- 
ducing, as an intermediate stage, a double effect, so that opposite processes 
seem to be consecutively induced by one and the same exciting cause. It 
is possible that this fact may ultimately give a clue to an explanation of the 
mechanism of the reversal, but at present I am unable to suggest any such. 
It has been already pointed out that asphyxial excitation of constrictors 
is abolished by strychnine in a less dose than that required to abolish the 
constrictor effect from reversed depressor action. A larger dose is necessary, 
