Literature DB >> 8031498

Bilateral destruction of the ventrolateral orbital cortex produces allocentric but not egocentric spatial deficits in rats.

J V Corwin1, M Fussinger, R C Meyer, V R King, R L Reep.   

Abstract

Previous studies have implicated the ventrolateral orbital cortex (VLO) in spatial attention and orientation. Unilateral destruction of the VLO has been found to produce severe multimodal neglect to unilateral stimulation which is qualitatively quite similar to that found following unilateral destruction of either the medial agranular or posterior parietal cortices. A series of anatomical studies have shown that the VLO is reciprocally interconnected with both the medial agranular cortex and the posterior parietal cortex, which are involved in egocentric and allocentric spatial processing respectively. However, the role of the VLO in either egocentric or allocentric spatial processing has never been directly examined. The present study directly examined the role of the VLO in spatial learning by examining the effects of bilateral VLO destruction on performance in both egocentric (adjacent-arm maze task) and allocentric (cheeseboard task) spatial tasks. Subjects in either the cheese board task or the adjacent arm maze were given presurgical maze training and then were assigned to one of three surgical groups: a bilateral VLO group, a lesion control group which received bilateral destruction of the laterally adjacent lateral orbital cortex which has a quite different pattern of connectivity than the VLO, or a sham operated control group. The results indicated that the VLO operates were significantly impaired in the cheeseboard task (allocentric task) relative to controls, but displayed no deficits in the adjacent-arm maze (egocentric task), a pattern of results similar to those found for the posterior parietal cortex. The results of the present study strongly support the contention that the VLO is a component of the cortical circuitry for spatial processing in rodents.

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Year:  1994        PMID: 8031498     DOI: 10.1016/0166-4328(94)90010-8

Source DB:  PubMed          Journal:  Behav Brain Res        ISSN: 0166-4328            Impact factor:   3.332


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