286 BRAIN MECHANISMS AND LEARNING 



'activating' influences have been shown to operate in rostral cortical 

 areas upon repetitive excitation of vcntralis posterior, centre median 

 (rostral pole) or ineso-ventral intralaminar nuclei of thalamus in acute 

 experiments (Jasper, Naquet and King, 1955; Starzl, Taylor and Magoun, 

 195 1). It is reasonable to advance the working hypothesis that the same 

 nuclei participated ni similar responses acquired by chronic preparations. 

 A mechanism similar (in terms of general structures and influences 

 involved) to that surmised above was presumed to intervene in the 

 establishment of current conditioned reactions (Gastaut, 1959). No 

 information is available as to the manner whereby T eventually became 

 capable of selectively energizing these structures and specifically triggering 

 these patterns. 



Most features (method, similarity of absolute and learned effects, 

 inhibitions, EEG manifestations, etc.) of typical conditioning were present 

 in the learning process described here: if one considers that substraction of 

 pain (and not pain itself) acted as absolute stmiulus, this learned reaction 

 may be incorporated to the conditioned reflexes group (Konorski, 1946; 

 Zbrozyna, 1958). Terms 'excitatory' and 'inhibitory' are vague unless 

 referred to precise effects: in this respect, T influence was not homo- 

 geneous, appearing either inhibitory (in the sense that it revoked posture 

 and movements induced by SS) and excitatory (in the sense that it 

 provoked 'desynchronization'). 



SS produced behavioural maniicstations of pain and elicited potentials 

 on contralateral sensory cortex; on application of T, performance and 

 electrographic signs were altered. Before entering into the final considera- 

 tions, the unavoidable questionability of the following points should be 

 stressed, (i) The afflictive consequences of similar excitation in man plus 

 behavioural manifestations exhibited by cats when receiving SS favoured 

 the assumption that stimuli were basically painful subjectively; though 

 heavily significant, this evidence was not totally decisive, (ii) Participation 

 of cerebral cortex in pain perception is accepted currently in experimental 

 and clinical literature and it is therefore possible that at least part of the 

 evoked potentials was due to activation of pam-conducting afferent 

 fibres (Anguelergues and Hccaen, 1958; Melzack and Haugen, 1957); 

 this must be demonstrated conclusively, however, (iii) Tones reduced 

 evoked potentials and dns could in fact mean that their application blocked 

 afferent volleys on their way to or at the cortex; the possibility subsists, 

 however, that cortical waves were obliterated by way of some other type 

 of influence (that, for instance, modified the temporal pattern of and the 

 relationship between individual discharges), (iv) Finally and even if SS 



