366 Information Storage and Neural Control 



Dr. John made a noble effort to reduce all this to a single 

 quantitative picture by pointing out that an increase, say, in total 

 cellular RNA would bind more ions and thereby cut down intra- 

 cellular potassium which would slow the discharge of the neuron 

 membrane and the optimal frequency at which it would respond. 

 Explanations of this sort we eagerly welcome. Many workers are 

 engaged in such efforts to push understanding further. My own 

 feeling is that if one reduces the RNA change to a single overall 

 quantitative parameter, even if parceled out to different cell 

 regions or membrane areas, there does not remain the necessary 

 great specificity; but this is certainly a matter of opinion at the 

 moment. In any event, here are the active growing points of 

 experiment, as well as theory, in this field. 



I shall take a final moment to add to those facts already before 

 you a few new ones regarding fixation. Dr. Morrell referred to 

 our earlier work, paralleled independently by others, of giving 

 an animal a certain learning experience and then, after different 

 intervals, stopping the activity of the brain. We found that if 

 brain activity was stopped early enough, either by abrupt cooling 

 or by massive electric shock, there had not been time for the 

 experience to become fixed in the nervous system. A hamster or 

 rat given an electric shock within a few minutes of an experience 

 had no recollection of the experience; the animal learned nothing, 

 much like the retrograde amnesia of man after a concussion. The 

 fixation time so established was fifteen minutes, although changes 

 continued for fully an hour. To grapple more firmly with the 

 engram, we wished a more localizing preparation, but without 

 encroaching on MorrelTs elegant mirror spot technicjue in the 

 cortex. There has been much argument as to whether the cord 

 can or cannot fix experience, or learn. Chamberlain, Haleck, and 

 I decided to follow a clue provided by an Italian physiologist, 

 Di Giorgio, relating to enduring" postural asymmetries after uni- 

 lateral lesions in the cerebellum or other cephalad structure. 

 Many mammals show the phenomenon. We have used rats mainly. 



After an asymmetrical lesion, the right hind leg is, say, more 

 flexed, the left one more extended. Now, of course, if the cord is 

 cut, the asymmetric streams of descending impulses are stopped 

 and cord discharges should lapse back to symmetry. This is, 



