Abstract

The [14C]-deoxyglucose quantitative autoradiographic method was used to map the metabolic changes induced by electrical stimulation and electrolytic lesion of the rostral pole of the thalamic reticular nucleus in the rat brain. Unilateral electrical stimulation of the thalamic reticular nucleus induced the following changes in glucose utilization: (i) local enhancement of metabolic activity within the stimulated thalamic reticular nucleus, (ii) increase in glucose consumption in the ipsilateral thalamic mediodorsal, centrolateral, ventromedial and ventrolateral nuclei, as well as in the nucleus accumbens, (iii) bilateral depression of metabolism in the locus coeruleus, periaqueductal gray, ventral tegmental area, and medial habenula, as well as contralateral metabolic depression in the substantia nigra reticulata, compacta and in the ventral pallidum. Unilateral electrolytic lesion of thalamic reticular nucleus elicited metabolic depression in the ipsilateral thalamic mediodorsal, centrolateral, ventrolateral and ventromedial nuclei, and metabolic activation in the dorsal tegmental nucleus bilaterally. The existence of a descending thalamic reticular nucleus input to the periaqueductal gray is supported by the depressed activity measured in brain stem structures after thalamic reticular nucleus stimulation. The similar effects observed in the periaqueductal gray and substantia nigra contralateral to the stimulated thalamic reticular nucleus indicate a possible flow of information from one thalamic reticular nucleus to the contralateral basal ganglia via the periaqueductal gray. The opposite effects induced in the dorsal thalamic nuclei by thalamic reticular nucleus stimulation and lesion support the gating role of the thalamic reticular nucleus in the information flow between thalamus and cortex.

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