This is a competing continuation of a project to study amnesia resulting from damage to nuclei of the diencephalon. Many current theories of learning and memory stress the role of frontal cortex and limbic cortical areas (e.g. perirhinal and entorhinal cortex and hippocampus). In contrast Korsakoff's disease and similar amnesia result presumably from damage to thalamic nuclei. The previous 10-years of this project have shown that in a rodent model of thiamine-deficiency amnesia (similar to Korsakoff's), the critical lesions occurred in the intralaminar nuclei (ILn) of the thalamus. Results have suggested that reciprocal """"""""loops"""""""" connecting ILn with motor, prefrontal and limbic regions are critical to diencephalic amnesia. The project will pursue the role of the reciprocal connections with motor, prefrontal and limbic brain areas first by selective lesions targeted at restricted regions of ILn associated with projections to and from each brain area. Second, the experiments will compare lesions of prefrontal cortex and striatum with ILn lesions to determine the role of reciprocal cortico-basal ganglion projections in amnesia. Third, the role of hippocampal projections will be determined by lesioning the perirhinal cortical and thalamic sites of hippocampal projections. Finally, lesions of the projection targets (prefrontal cortex and hippocampus) will be compared with results indicating that ILn lesions (similar to Korsakoff's disease) cause a slowing of reaction time in a serial reaction task.
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