182 



N. CHALAZONITIS 



cells that are initially autoactive, the anoxic depolarization leads to cessation 

 of autoactivity. This inhibition appears to be the result of excessive de- 

 polarization.* 



The latencies required for anoxic inhibition of these cells are given in 

 Table 1. 



Table 1 



A careful analysis of the inhibition by anoxia of the Br cell shows that: 



(a) The presence of oxygen is required for the periodical repolarization of 

 the cell (positive phase of the slow wave. Fig. 2). 



(b) Generally a 2-min anoxia (under nitrogen) at 20'C is sufficient to abolish 

 the activity by "trains" because the positive phase of the slow wave is abol- 

 ished; the resulting activity becomes a steady spike discharge. If we regard 

 the positive phase of the slow wave as a normal periodical inhibition, such 

 primary anoxic effect may be considered as an "inhibition of an inhibition". 

 Under such conditions the Br cell behaves as an A cell, namely, it fires at a 

 constant, regular frequency. 



(c) Finally, after four more minutes of anoxia the activity of the Br cell 

 degenerates into damped oscillations and the cell stops firing. 



The evolution of the A cell activity under anoxia is different. As anoxic 

 depolarization begins, the frequency of the A cell first increases, and then, 

 after a total depolarization from 10 to 15 mV, the cell stops firing. 



The slow effect of anoxia on the activity of arhythmic cells (B or Gen or 

 sometimes p.c.r.) is not yet clearly understood. These cells are less sensitive 

 to anoxia than are the cells discussed above, and this is probably due to their 

 ceaseless synaptic repolarization by spontaneous inhibitory (hyperpolarizing) 

 neurons. 



A possible interpretation of the anoxic inhibitory effects on the soma, 



observable after the initial excitatory effects, is that the anoxia, at least in 



some cells, causes an excessive depolarization. 



* See also Eyzaguirre and Kuffler (1955) and Granil and Phillips (1956) relating 

 inhibitory effects by excessive depolarization. 



