54 METABOLISM IN CHANGED CEREBRAL ACTIVITY 



e.e.g. before any changes in levels of phosphocreatine could be 

 measured. How^ever, it is to be remembered that observations of 

 this type do not necessarily mean that electrical activity of the 

 brain is associated more closely w^ith an oxidative rather than w^ith 

 a phosphorylative mechanism. Disappearance of spontaneous 

 electrical activity before the breakdow^n of phosphocreatine is 

 detectable may w^ell mean that phosphocreatine is at one end of a 

 chain of reactions, the other end of v^^hich is intimately connected 

 v^ith the changes leading to electrical disturbances. The quantity 

 of a phosphate in a tissue is not a reliable indication of its rate of 

 metabolism and situations such as above appear to offer considerable 

 scope for investigations with radioactive phosphate. 



Electroshock and Convulsive Agents 



The simplest method of administering a major shock to the 

 brain is by decapitation which severs the spinal cord and at the 

 same time stops the supply of oxygen and glucose. Such a pro- 

 cedure results in an almost immediate decrease in the quantities 

 of cerebral phosphocreatine and an increase in the levels of 

 inorganic phosphate (Table 10). These changes are not wholly due 

 to stimulation associated with decapitation since they do not occur 

 if the head is allowed to fall into liquid nitrogen within 1-2 sec (see 

 Table 1). The changes, however, are rapid and take place within 

 3 sec of decapitation. Several minutes later, if the brain is left 

 unfrozen, the increased quantities of inorganic phosphate far 

 exceed the decrease in the quantities of energy-rich phosphate, a 

 situation similar to that after prolonged anoxia or severe ischaemia. 



Experiments such as these, though demonstrating extreme 

 promptness of cerebral reactions, do not permit the separation of 

 the effects of stimulation from those of anoxia and hypoglycaemia. 

 This separation is essential in analysing the effects of convulsant 

 agents. In early experiments, Kerr and Antaki (1937) failed to 

 find any difference from normal in the quantities of phospho- 

 creatine in the brains of animals convulsed by picrotoxin. How- 

 ever, the animals were anaesthetized with sodium amytal before 

 freezing the brain, a procedure now recognized as sufficient to 

 nullify changes which had taken place. The technique more 

 widely adopted is that due to Stone et al. (1945) which permits the 

 study of chemical changes in the cortex during convulsive activity 



