Effects of selective destruction of the dorsal central striatum on directed attention in rats
Van Vleet, Thomas M.
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The neglect syndrome is a complex and devastating disorder characterized by spatial and attentional deficits, lack of affect, and unresponsiveness to the side of space opposite a brain lesion. A rodent model of neglect has been developed in order to examine the neural mechanisms underlying neglect. Unilateral destruction of the medial agranular cortex (AGm), which projects into the dorsocentral and dorsolateral striatum, produces severe neglect. A number of studies have found changes in striatum that are correlated with behavioral recovery from neglect. Physiological studies have indicated that neglect induced by AGm destruction is correlated with reductions of metabolic activity in the dorsolateral quadrant of striatum, which includes the dorsal central striatum. Further, spontaneous recovery is associated with normalization of metabolic activity in the dorsal central striatum. In addition, asymmetries in striatal immediate early gene expression have been correlated with neglect induced by AGm destruction. The present study directly tested these correlational findings by examining the behavioral effects of unilateral destruction of the dorsocentral striatum. The objective of the present study was to determine the importance of the dorsocentral striatum in the system for directed attention in the rat. Three experimental groups were used: a dorsocentral striatum NMDA lesion group, a ventral lateral striatum NMDA lesion group, and a dorsocentral striatum vehicle group. Subjects were tested for neglect 2 days post-lesion and three times per week for the following three weeks. The results showed that the dorsocentral striatum lesion group demonstrated more severe neglect than the ventral lateral striatum lesion and saline control groups. The results of the present study suggest that the dorsocentral striatum is an important component of a corticosubcortical network involved in neglect and directed attention.