1 90 Information Storage and Neural Control 



focal epileptogenic lesions prevent new learning, i.e., impair 

 memory recording, but do not disturb behavior learned before 

 establishment of the epileptic lesion (31, 34, 35, 42, 51). 



A limiting case in the requirement for a finite fixation time is 

 the classical example of one-trial learning. However, even in this 

 instance, it has been supposed (Hebb) (24) that the neural con- 

 sequences of the single experience persist in the form of rever- 

 berating impulses for a considerable time after the environmental 

 signal has ceased. x\lthough all or none impulses circulating in 

 closed neuronal chains represent one possible mechanism for the 

 initial imprinting or short-term memory the actual kind or kinds 

 of electrical activity involved remain unknown. In fact, there is 

 nothing in the experimental evidence concerned with manipula- 

 tion of the consolidation process which affords compelling proof 

 that consolidation depends upon reverberating impulses of the 

 all or none type (41). Other kinds of electrical activity, that is, 

 other than the classical axon spike or even the conventionally 

 recorded EEG may well be equally important. 



I should like to present some evidence which suggests that 

 cortical steady potential gradients may have a determining in- 

 fluence in the process wherein a sequence of impinging impulses 

 is transformed into structural change in the nervous system. This 

 portion of the paper, therefore, is concerned with the initial or 

 electro-sensitive stage of memory recording. 



Significant shifts of the cortical steady potential have been shown 

 to occur consequent to stimulation of peripheral receptors (19) as 

 well as when stimulating electrodes are applied directly to brain 

 substance (2, 7, 8, 9, 16, 17, 18). Some years ago, we found (37) 

 that the surface negative DC shift resulting from low frequency 

 stimulation of nucleus centrum medianum in the thalamus would 

 appear as a conditioned response to a pure tone after thirty to 

 forty paired trials. 



Figure 1 illustrates the first paired trial. The tone elicited no 

 response. Upon onset of the thalamic stimulus, a pronounced 

 negative shift of the base line of the EEG occurred, which was 

 confined to the hemisphere ipsilateral to the stimulated site. 

 After about forty paired trials (Fig. 2) a similar DC shift was 

 regularly induced by the tone alone. Note particularly that this 



