E. GRASTYAN 261 



only in a record ot Stage II. In Stage 1 both mesencephalic reticidar formation and 

 the hippocampus show increased discharge. Thus the relation between hippo- 

 campal and reticular discharge could not be described as reciprocally inhibitory 

 but rather changed with change in stage of conditioning. On the other hand, the 

 evidence does support the contention of Gastaut (1958) and Yoshii (1957) that 

 participation of elements in the thalamic reticular system is essential for the fmal 

 development of a conditioned response and that some form of thalamo-cortical 

 linking forms the substrate of a iully developed learned response. As Dr Grastyan 

 has already noted, our results as well as his own, tend to support the impression of 

 John and Killam (1959) with respect to the particular role of the hippocampus in 

 the early stages of conditioning. 



In different ways it would appear that both hippocampus and mesencephalic 

 reticular formation are concerned in the initial steps which determine what events 

 will or will not become crystallized as engram. In no case where this entire sequence 

 has been observed did the thalamo-cortical linkage appear without prior activity 

 in hippocampal and mesencephalic systems. Of particular interest was the fact that 

 definite inhibitory sequences were always evident (in the form of suppression of 

 resting unit discharge) in the course of acquisition of the simple positive temporary 

 connection. The fact that these inhibitory unit events were highly correlated with 

 the development of the so-called frequency-specific repetitive response in the 

 gross surface electrical tracing may help explain the lack of correlation between 

 this particular electrical manifestation and behavioural transfer. 



It may well be that these conditioned changes in discharge patterns of single 

 nerve cells are a different order of phenomenon from that understood as be- 

 havioural learning. Yet it would seem that ultimately alterations in behaviour of 

 the total organism must be related in some way to changes in behaviour of nerve 

 cells. It is in this sense and in this context that we believe that we can demonstrate 

 learning (defined as a change in discharge frequency consistently related to an 

 experimentally imposed signal pattern) in single cells of the central nervous system. 



JouvET. Dr Grastyan, I agree with you that extinction of the orientating reflex 

 may come from some upper level. I have also been studying extinction of orienta- 

 tion reflex in chronic decorticate cats and in chronic mesencephalic cats. I could 

 never habituate the startled response in decerebrated animals. Sometimes after as 

 many as 800 stimuli I still obtained startled responses. Concerning decorticate cats 

 but with paleocortex remaining, I could not get a true extinction of orientation 

 reflex and in other cats after removing the frontal lobes I found that this also would 

 cause a disturbance in the extinction of the orientation reflex. I expect to show that 

 this inhibitory influence may come mainly from the neo-cortex and from the 

 frontal lobes. I think this is in agreement with Dr Konorski. But of course there 

 must be some relationship between the hippocampus structure and the diffuse 

 thalamic nuclcii. I feel that the cortex is absolutely necessary, at least some part of 

 it, for this inhibition ot the orientation reflex. 



Hebb. One of the things that arouse orientation is the 'strange' object. But it is 

 not one that has never been presented before. It acquires its capacity to arouse. 

 This is seen clearly in Riesen's chimpanzees reared in darkness. The visual event in 

 the form of a light flash, would produce a startle response; but otherwise the visual 

 event, which by definition was strange, had no capacity at all to produce an orienta- 

 tion reflex. The tenor of Dr Grastyan's paper is that we need pay attention to the 



