434 GUSTAF FR. GOTHLIN 
assume that the inhibitory effect is connected with a formation 
which has its function reduced by the poison earlier and to a 
greater extent than the conductive bridge between the swimming 
plates. From a pharmacodynamic point of view, a formation of 
this kind, more sensitive to poison, can scarcely be anything else 
but a nervous conductive path, as narcotic poisons in the lowest 
concentrations affect nervous elements especially. 
Experiments 7 and 8 show that atropin in concentrations that 
are greater than 3:10,000 has a marked influence on the ciliary 
apparatus. This influence is complicated, however, by the fact 
that the atropin also elicits contractions of the animal’s body 
with secondary inhibition of the ciliary motion. If one man- 
ages, however, to observe an atropin-poisoned animal during the 
intervals between these contractions (experiment 8) one finds the 
frequency of the ciliary motion increased. If, also, during one 
of these intervals, one conveys a longitudinal oro-central cur- 
rent of the density that totally inhibits the ciliary motion in the 
rows of a normal animal, the effect proves to be (experiment 8) 
the same as in isolated, spontaneously striking swimming plates 
of the animal, i.e., an increase in the frequency of vibration. 
This increase can be observed right up to the density of current 
at which the threshold for the secondary inhibitory mechanism is 
reached and the animal contracts convulsively. 
From these observations one may conclude that atropin in 
the degree of concentration mentioned reduces the irritability of 
and probably gradually completely paralyzes the primary inhibi- 
tory mechanism which in a normal animal is so easily caused to 
function by a longitudinal oro-central current. It is also note- 
worthy with regard to atropin that the paralysis of the inhibi- 
tory mechanism under its influence is developed decidedly more 
slowly than the corresponding paralysis caused by chloral hydrate 
(experiment 8 compared with experiment 4) and that, when the 
animal is put back again into fresh sea-water this paralysis dis- 
appears so slowly. On account of this, one is tempted to assume 
that the atropin must enter into some chemical combination in 
the tissues in order to be effective. 
