METABOLISM IN CHANGED CEREBRAL ACTIVITY 59 



dioxide content of the air breathed, Bain and Klein (1949) 

 administered air/carbon dioxide mixtures to cats treated with 

 metrazole. In such animals breathing 15% CO 2/85% Og there 

 was apparently no decrease in the levels of phosphocreatine though 

 these changes took place in animals breathing air. However, in the 

 dog, Gurdjian et al. (1947) found that administration of up to 

 70% CO 2 with oxygen failed to prevent the decrease in phospho- 

 creatine levels which occurred during metrazole seizures. A 

 similar result was recorded following a 10 sec electroshock given 

 to a monkey breathing 30% CO 2/70% O2. Cerebral phosphates 

 changed as in the animals breathing air (Bain et al., 1949). Carbon 

 dioxide is known to increase the rate of cerebral blood flow and in 

 those instances where its presence has prevented a decrease in the 

 levels of phosphocreatine it seems reasonable to assume that the 

 increased oxygenation of the tissue assists in the adequate main- 

 tenance of phosphate levels (cf. Bain and Klein, 1949). 



Even in the absence of added carbon dioxide not all convulsive 

 activity or convulsive agents produce a marked decrease in cerebral 

 phosphocreatine. Thus, in rats, following brief electroshock 

 (Dawson and Richter, 1950(2), convulsions were accompanied by a 

 steady resynthesis of phosphocreatine, the convulsions ceasing 

 when the normal level was regained. In rats in which convulsions 

 were induced with fluorocitrate (Dawson and Peters, 1955), the 

 levels of phosphocreatine, though decreasing by a statistically 

 significant amount were not depleted sufficiently for the authors to 

 consider the changes as being meaningful. Convulsions are the end 

 point, or manifestation, of a series of changes which have already 

 taken place and in such conditions the brain may not always show 

 changes in levels of cerebral phosphates. In the dog, seizure 

 activity of the cortex induced by fluoroacetate (which is converted 

 to fluorocitrate) was accompanied by a decrease in phosphocreatine 

 and an increase in inorganic phosphorus during the seizure, the 

 pattern paralleling that induced by metrazole. In the period of 

 post seizure depression with intermittent convulsions phospho- 

 creatine decreased to 0- 1-0-3 [x moles /g wet wt. and adenosine 

 triphosphate also decreased by about 60%. The results were not 

 attributed to hypoxia caused by a block of oxidative pathways since 

 citrate accumulated in the precortical seizure period yet levels both 

 of lactate and of phosphocreatine remained normal (Pscheidt, 

 et al, 1954). 



