Functional anatomy of the thalamic centrolateral nucleus as revealed with the [14C]deoxyglucose method following electrical stimulation and electrolytic lesion.

Abstract

The effects of electrical stimulation and electrolytic lesion of the thalamic intralaminar centrolateral nucleus were studied in the rat brain by means of the quantitative autoradiographic [14C]deoxyglucose method. Unilateral electrical stimulation of the centrolateral nucleus induced: (i) local increase in metabolic activity within the stimulated centrolateral nucleus and the ipsilateral thalamic mediodorsal nucleus, (ii) metabolic depression in all layers of the ipsilateral frontal cortex, (iii) bilateral increase in glucose consumption within the periaqueductal gray, pedunculopontine nucleus, and pontine reticular formation, and (iv) contralateral metabolic activation in the deep cerebellar nuclei. The unilateral electrolytic lesion of the thalamic centrolateral nucleus elicited metabolic depressions in several distal brain areas. The metabolic depression elicited in the mediodorsal, ventrolateral, and lateral thalamic nuclei, as well as in the caudate nucleus, the cingulate, and the superficial layers of forelimb cortex were ipsilateral to the lesioned side. The metabolic depression measured in the medulla and pons (medullary and pontine reticular formation, periaqueductal gray, locus coeruleus, dorsal tegmental, cuneiformis, raphe and pedunculopontine tegmental nuclei), the cerebellum (molecular and granular layers of the cerebellar cortex, interpositus and dentate nuclei), the mesencephalon (substantia nigra reticulata, ventral tegmental area and deep layers of the superior colliculus), the diencephalon (medial habenula, parafascicular, ventrobasal complex, centromedial and reticular thalamic nuclei), the rhinencephalon (dentate gyrus and septum), the basal ganglia (ventral pallidum, globus pallidus, entopeduncular and accumbens nuclei) and the cerebral cortex (superficial and deep layers of the frontal and parietal cortex, deep layers of the forelimb cortex) were bilateral. These functional effects are discussed in relation to known anatomical pathways. The bilateral effects induced by the centrolateral nucleus lesion reflect an important role of the centrolateral nucleus in the processing of reticular activating input and in the interhemispheric transfer of information. The cortical metabolic depression induced by centrolateral nucleus stimulation indicates the participation of this nucleus in attentional functions.