H. ENGER ROSVOLD AND MORTIMER MISHKIN 567 



hypotheses were derived. On this basis it would seem profitable to begin 

 exploring other possibilities and not contme ourselves to the one class of 

 theoretical concepts. 



To summarize the major points of this analysis: A survey of the older 

 literature, reinforced strongly by recent evidence, has shown that with 

 certain conditions of testing frontal lesions produce severe impairment m 

 learning and performance on discrimination tasks in all sensory modalities. 

 An explanation of this deficit in terms of a sensory-perceptual loss w^as 

 rejected in favour of a non-sensory loss specific to frontal lobe damage. 

 While much of the evidence favours an interpretation of the impairment 

 as a loss of inhibition, a careful examination of three specific types of 

 proposed inhibitory defects shows that none of them satisfactorily 

 accounts for all of the data. In further work directed towards the elucida- 

 tion of the frontal animals' non-sensory impairment, an important problem 

 will be to determine what relationship, it any, the deficit oi the frontal 

 animal on discrimination tasks bears to its deficit on delayed-response 

 tasks, the symptom which has traditionally guided theory and research 

 concerning frontal lobe function. 



GROUP DISCUSSION 



Disiiiliihifion of inhibitory CRs after prefrontal lesions in doos 



KoNORSKi (written comment). Since our laboratory has been directly con- 

 cerned with the problem of the impairment of inhibitory processes after prefrontal 

 lesions for nearly 10 years, I should like to present very briefly our experimental 

 material dealing with this subject and, with our results as a basis, to comment on 

 some of the statements put forward by Rosvold and Mishkin in their paper. 



Our work has been performed on dogs in which we established various types of 

 excitatory and inhibitory CRs ; then we removed, to varying extents, the prefrontal 

 areas (or as a control some parts of the parietal areas) and observed the changes in 

 CRs for a long time after these operations. Inhibitory CSs were either stimuli 

 similar to the positive CSs (differentiation) or were compounds composed of a 

 positive CS preceded bv another stimulus (so called conditioned inhibition). 

 Inhibitory stimuli were, of course, not reinforced by any UCS. 



Prefrontal lesions consisted of amputation of the frontal poles rostral to the 

 prcsylvian sulcus; in this way gyrus proreus, gyrus subproreus and the anterior 

 part of gyrus orbitalis, as well as subjacent white matter, were removed. Parietal 

 lesions consisted of removal of parts of gvrus entolateralis and suprasplenialis 



In Table I the results obtained in these experiments are summarized. As seen 

 from this table, after prefrontal lesions positive CRs are either normal or enhanced, 

 while inhibitory CRs are disinhibited. This holds true with respect to both ali- 

 mentar)- (food and water) and defensive (electric shock and acid) reflexes. Only in 



