Abstract
A thalamo-cortical system with origins in the midline nonspecific thalamic nuclei and projections to the orbitofrontal granular cortex has been identified with an electrocortical synchronizing function related to internal inhibition. 30 acute and 14 chronic cat preparations have been utilized in the study of the nonspecific thalamo-cortical system, including its origins, pathways and cortical projections. Its functional role has been assessed in terms of its effect upon spindle bursts, recruiting and augmenting responses, sensory evoked potentials and the performance of certain learned behavioral tasks. Interruption of this nonspecific thalamo-cortical system has been produced by lesions or reversible cryogenic blockade, and by cortical ablations at 3 principal sites: n. ventralis anterior, the inferior thalamic peduncle (ITP), and the orbitofrontal cortex. Blockade of this thalamo-cortical synchronizing mechanism has resulted in 3 effects: (1) Reduction or abolition of recruiting responses elicited by stimulation of the midline thalamic nuclei, and reduction or abolition of spontaneous spindle bursts produced by lesion of the mesencephalic reticular formation. These effects involving the nonspecific thalamo-cortical system are contrasted with the specific sensory and motor systems whose augmenting responses are not affected by blockade of the thalamo-cortical system. (2) Enhancement of visual cortical responses elicited by photic or optic tract stimulation. This effect upon specific sensory responses contrasts with the reduction or abolition of spindle bursts and recruiting responses mediated by a nonspecific system. (3) Deficits in performance of learned behavioral tasks involving bar-pressing and single alternation. Complete cryogenic blockade in ITP interrupted bar-pressing whereas partial blockade only slowed bar-pressing rate but interfered with single alternation performance due to perseveration. The nonspecific thalamo-cortical system has been discussed in terms of its synchronizing and regulating influences upon electrocortical activity, its inhibitory role, and as a possible mechanism mediating attention and inattention.
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