FACTORS AFFECTING THE SUSCEPTIBILITY OF FROGS TO THE CONVULSANT ACTION OF ACID FUCHSIN

¹ From the Department of Physiology of Saint Louis University School of Medicine

This study has been primarily a search for evidence either for or against the view originally expressed by Barbour and Abel (1) that the increase in susceptibility to acid fuchsin in frogs after decerebration was due to the failure, because of decerebration, of a previously functional inhibitory mechanism.

1. It was found that removal of one cerebral hemisphere was as effective as complete decerebration in increasing the susceptibility of frogs to acid fuchsin.

2. The presence of one uninjured cerebral hemisphere failed to alter either the character or the time of appearance of convulsions when compared with the results of complete decerebration.

3. The following procedures have also been shown to increase definitely and markedly the susceptibility of frogs to the convulsant effects of acid fuchsin:

a. Injuries to the olfactory lobes.

b. Injuries to the brain which were considered to be too slight to interfere seriously with function, such as simple needle punctures.

c. Injuries to the spinal cord including both transection and needle punctures.

d. Deep etherization, in which respiration ceased for a time.

4. After transection of the spinal cord at the level of the inferior angles of the scapulae the head end of the body was involved in convulsions before the posterior end, in spite of the fact that the cerebrum was uninjured and therefore should have been able to delay the onset of convulsions if the delay seen in normal frogs is due to inhibition.

5. The fact that injuries of such a wide variety, some of them (b) probably too slight to interfere seriously with function, cause an increase in the susceptibility of the frog to acid fuchsin similar in character to that produced by complete decerebration, speaks strongly against the view that the increase in susceptibility after complete decerebration is due to damage to a hypothetical inhibitory mechanism in the cerebrum. The question of the existence or non-existence of an inhibitory mechanism in the cerebrum is not the question at issue in this communication for the experimental methods used by both Barbour and Abel and myself are probably not suitable to decide that question.

6. It seems clear, therefore, that we are not dealing here with a factor of cerebral inhibition and that the conclusion previously drawn (3), to the effect that "cerebral inhibition is a minor factor, if it is a factor at all, in determining the time of onset of acid fuchsin convulsions" was fully warranted.