H. ENGER ROSVOLD AND MORTIMER MISHKIN 573 



As to the third possibihty proposed by the authors (loss of stiniukis inhibition 

 manifested by hyperreactivity) I would rather doubt whether it exists at all, since 

 we have no conclusive evidence that prefrontal animals arc more distracted by 

 extraneous stimuli than are normal animals (cf. the experiments by Butler and 

 Harlow (1956) in which no increased distractability was found, after prefrontal 

 lesions in monkeys). The detrimental effect of extraneous stimuli in prefrontal 

 animals in the delayed-responsc test is simply due, as we have shown, to the fact 

 that these animals must keep their bodily orientation unchanged during the delay 

 in order to perform the correct response. Since an extraneous stimulus may provoke 

 a change in orientation (just as it docs m normal animals), so correct dclayed- 

 response performance is impossible for prefrontal annuals, while normal animals, 

 not having to maintain their orientation during the delay, are unaffected. 



RosvOLD and Mishkin (written rebuttal submitted as afterthought). In his 

 discussion of our paper, Konorski has presented evidence which seems to support 

 the view that limited prefrontal lesions produce what we have referred to as a loss 

 of 'drive inhibition'. Let us re-examine the hypothesis in terms of this evidence first. 



According to Konorski, the instrumental response to a negative (unrewarded) 

 stimulus is normalh' inhibited by both drive and response inhibition. For con- 

 venience we shall call the sum of their effects the (total) inhibitory tendency. Now 

 if a limited prefrontal lesion impairs drive inhibition, but leaves response inhibition 

 intact, then the total inhibitorv tendency should be reduced but not eliminated. 

 Yet, in the experiments on auditory differentiation, the animal's inhibitory response 

 is not simply weakened by the lesion ; it is transformed into an excitatory response. 

 Thus it seems to us that the drive disinhibition hypothesis does not account satis- 

 factorily even for data that have been presented to support it. Hut perhaps this 

 difficulty can be avoided by making some additional assumption, e.g. that normally 

 the total inhibitory tendency depends primarily on drive inhibition, and when this 

 is impaired, sufficient drive excitation is released to overcome the intact, but 

 relatively weaker, response inhibition. In this way, a strong inhibitory response 

 might be transformed by the lesion into, at least, a weak excitatory response. While 

 it is hardly our wish to defend it, let us for the moment accept some such explana- 

 tion of the impairment in auditory differentiation (in which stimuli are presented 

 successively) and turn next to the experiments on visual discrimination with simul- 

 taneously presented stimuli. 



In simultaneous discrimination, as opposed to differentiation, impairment after 

 frontal damage has rarely been observed. Konorski suggests a simple explanation: 

 When both positive and negative stimuli are simultaneously present, the strong 

 excitatory response which was conditioned to the positive stimulus before opera- 

 tion will still predominate after operation. This will be true whether the inhibitory 

 tendency to the negative stimulus is now merely reduced, or, according to our 

 added assumption, changed into a weak excitatory tendency. But while this 

 explanation will account for the successful retention of a simultaneous-discrimina- 

 tion habit, we do not believe it will account for successful post-operative learning. 

 When a frontal animal is trained only after operation, an impairment of drive 

 inhibition should retard the development of an inhibitory tendency to the negative 

 stimulus, and thereby delay the appearance of a predominant response to the 

 positive stimulus. In short, discrimination learning should be impaired. Numerous 

 experiments have indicated that, contrary to such a prediction, the frontal animal 



