AN EXAMINATION OF THE HYPNOTOXIN THEORY OF SLEEP

Publisher Website
Google Scholar
Abstract
9 of 20 dogs in which 8 cc. of cerebrospinal fluid were withdrawn during 3 mins. and then replaced by an equal quantity of cerebrospinal fluid from dogs kept awake in standing position for from 7 to 16 days showed a depression of the central nervous system or "sleep" which was graded either 3 or 4 plus. Only 4 of the 24 control dogs which received in the same manner either fluid from a normal dog or their own fluid or normal saline soln. showed a 3 plus depression and none a 4 plus depression. To this extent the observations of Pieron were confirmed. The normal picture of sleep was not produced, because the body temp. of both groups of animals was elevated approximately 2.6[degree] F. Further the cerebrospinal fluid pressure was elevated, the maximum elevation being to approximately 44 cm. of normal saline soln. The simple withdrawal and reinjection (warmed syringe) of 8 cc. cerebrospinal fluid during a period of 6 mins. caused a rise in ventricular pressure and body temp. in anesthetised dog. The elevated intracranial pressure was probably a factor which operated to augment the depression that occurred after the cisternal inj. of cerebrospinal fluid from a fatigued dog, because the intraven. inj. of hypertonic glucose decreased the degree of depression for a 20 or 30 min. period. A rise in intracranial pressure could not be a feature of prime importance in causing the onset of sleep because when 8 cc. of cerebrospinal fluid were withdrawn from a fatigued dog, such a dog fell into a profound sleep within 5 mins. The withdrawal of a similar quantity of fluid from a non-fatigued dog did not cause sleep or objective changes. A detailed assay of the cerebrospinal fluid of fatigued dogs might yield results which would reflect the underlying chemical changes which led to fatigue and were conducive to sleep. Acetylcholine could not be detected in the cerebrospinal fluid of normal or fatigued dogs. The possibility that fatigue interfered with the "chemical mechanism for the transmission of nerve impulses" was not ruled out by the results of our study of the acetylcholine mechanism.

This publication has 1 reference indexed in Scilit: