Abstract

Recent study has revealed a cephalically directed brain stem system whose stimulation desynchronizes the electrical activity of the cerebral cortex in a manner simulating that observed in awakening from sleep or in the EEG arousal reaction (8). This system was found to be distributed in the reticular formation of the medulla, the tegmentum of the pons and midbrain and the sub- and hypothalamus. The means by which its activating influence became exerted upon the cortex was speculated upon and, because of the generalized distribution of the cortical effects, it seemed likely that the diffuse thalamic projection system was concerned. Some evidence favoring this possibility was obtained but the problem was left for further investigation. Following preliminary determination of the organization of the diffuse thalamic projection system (12), the present study has explored this matter further: (i) by determining the thalamic regions whose electrical activity is desynchronized by stimulation of the reticular formation of the lower brain stem, (ii) by determining the distribution of thalamic sites from which evoked potentials are recorded upon single shock stimuli to the reticular activating system, (iii) by exploring the thalamic areas whose direct excitation desynchronizes the electrocorticogram, (iv) by ascertaining the distribution of cortical potentials evoked by single shock stimulation of the reticular activating system, and (v) by determining the effect of diencephalic lesions on ascending conduction of the reticular influence. The results indicate that the ventromedial part of the thalamus is most critically involved in transmission of the reticular activating influence, with the rest of the thalamus (including the diffuse thalamic projection system) playing a subsidiary role. Evidence, moreover, is provided that a proportion of the influence of the reticular activating system upon the cortex may be exerted by an extra-thalamic route, paralleling that of the secondary response system described by Morison et al. (1, 10, 11).

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