H. ENGER ROSVOLD AND MORTIMER MISHKIN 57I 



representations of the CS and UCS, alongside the excitatory connections formed 

 earlier between these two representations. The prefrontal lesion may either destroy 

 these inhibitory connections leaving the excitatory connections unaffected, or else 

 it may, by some unspecific release mechanism (reticular formation?), increase the 

 excitability oi unconditioned centres [both appetitive and defensive) and in this 

 way give predominance to excitatory over inhibitory impulses. Irrespective of 

 which of these two alternatives (if any) proves to be correct we have here to do 

 exclusively with the phenomenon labelled by Rosvold and Mishkin as loss of drive 

 inhibition: this is obvious for those experiments in which classical CRs were used; 

 as tor those experiments in which instrumental reflexes were used it could be 

 shown that disinhibition of instrumental responses faithfully reflected disinhibition 

 of the salivary response, i.e. oi the ahmentary drive (Brutkowski, 1959). 



I cannot agree with Rosvold and Mishkin's argument that the results obtained 

 by Weiskrantz and Mishkm (195M) with a 'go-no go' symmetrical reward schedule 

 to two different sounds arc contradictory to the drive disinhibition mechanism. 

 These authors found that after prefrontal lesions a 'no-go' response is disinhibitcd 

 in spite of the tact that it is rewarded. But we know from the vast experimental 

 evidence of the Pavlov school, as well as from our own experimental data (Konor- 

 ski and Szwcjkowska, 1952), that even the repeated reinforcement of an inhibitory 

 stimulus may not lead to its transformation into a positive stimulus. The stimulus to 

 which the animal was to refrain from responding in order to obtain tood was 

 deeply extinguished at the beginning of trainnig, since the animal repeatedly 

 performed the trained movement to it and did not get food; as a result this 

 stimulus probably could not be tully established as a positive CS when, after the 

 instrumental response to it had been inhibited, the animal was reinforced. Had the 

 authors measured salivation, the}- could have checked whether or not this supposi- 

 tion is correct. According to the view that the prefrontal lesions did produce drive 

 disinhibition oi inhibitory alimentary reflexes, the inhibitory stimulus became 

 excitatory, which was reflected in the animal's performing the learned movement 

 to it. 



Similarly, it seems to me that the argument ot the authors pointing out that 

 simultaneous-discrimination habits should be impaired by drive disinhibition is 

 also not correct. The animal is presented simultaneously with two objects, the 

 reaction to one of them being constantly reinforced. As a result tliis reaction be- 

 comes much stronger than the reaction to the other object since the latter reaction 

 is inhibited both by drive and response inhibition. There is, therefore, no reason 

 why atter a prefrontal lesion the first reaction should not predominate. 



Yet, we Imvv tound that after larger prefrontal lesions which include the pre- 

 cruciate areas a new phenomenon ensues which may be defined as 'motor- 

 response disinhibition'. After these lesions the animals not only exhibit locomotor 

 hyperactivity, but also, when put into the experimental situation in which a 

 definite instrumental CR had been established, they perform the trained movement 

 again and again apparently without any relation to the hunger drive (Fig. 2C; 

 Konorski, 1957). It is worth mentioning that this sort of disinhibition is, like the 

 first one, 'conditioned'. In one dog, two different instrumental responses were 

 trained in two different situations; after the more extensive prefrontal lesion this 

 dog manifested hyperactivity ot the motor reaction specific to the given situation 

 and not to the other one. 



