Unilateral destruction of the dorsocentral striatum in rats produces neglect but not extinction to bilateral simultaneous stimulation

A number of previous studies have indicated that lesions of the medial agranular cortex (AGm) in rats induce multimodal neglect and extinction to bilateral simultaneous stimulation (extinction), the two major symptoms of the neglect syndrome in humans. A recent study demonstrated that lesions of dor...

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Veröffentlicht in:Behavioural brain research 2002-11, Vol.136 (2), p.375-387
Hauptverfasser: VanVleet, T.M, Heldt, S.A, Guerrettaz, K.R, Corwin, J.V, Reep, R.L
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Sprache:eng
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Zusammenfassung:A number of previous studies have indicated that lesions of the medial agranular cortex (AGm) in rats induce multimodal neglect and extinction to bilateral simultaneous stimulation (extinction), the two major symptoms of the neglect syndrome in humans. A recent study demonstrated that lesions of dorsocentral striatum (DCS), the site of AGm projections to the striatum, produce multimodal neglect qualitatively similar to that found with AGm lesions. In the present study, the behavioral effects of unilateral DCS lesions were examined in more detail for the major manifestations of neglect: hemineglect, extinction, and allesthesia/allokinesia. Subjects were tested for extinction to bilateral simultaneous stimulation of the forepaws three times a week for 3 weeks. Neglect testing occurred twice weekly and the subjects were tested for the presence of neglect by rating the magnitude of orientation to visual, tactile, and auditory stimulation. The results indicated that DCS operates, while demonstrating severe neglect, failed to demonstrate extinction or allesthesia/allokinesia. These findings suggest that the neural mechanisms that underlie neglect and extinction are dissociable in this system. A better understanding of the neural mechanisms that underlie extinction is particularly important because humans that have recovered from neglect often continue to demonstrate the debilitating symptoms of extinction.
ISSN:0166-4328
1872-7549
DOI:10.1016/S0166-4328(02)00296-6