In the clinic, one commonly encounters patients who are amnestic. These patients and their families often complain that the patient is unable to remember. These patients often demonstrate antegrade amnesia and are unable to learn new verbal and/or nonverbal information. AMnesia may be associated with a wide variety of diseases including primary degenerative dementia, strokes, head trauma and alcoholism. The major output of the hippocmapal system is by way of the subiculum. The subiculum projects to both the fornix and retrosplenial area. Recently, we examined and studied a profoundly amnestic patient with a lesion in the retrosplenial area. This lesion, however, may have also damage the fornix. Lesions completely restricted to the retrosplenial area have not been reported to produce amnesia in humans and the one case with amnesia from a fornix lesion near the splenium may have, in retrospect, involved the retrosplenial area. We therefore cannot be certain if injury to either one or both of these structures is necessary to induce amnesia. One method of resolving this issue is to make selective lesions of these structures in animals and test memory using a delayed non- matching to sample task. This task is sensitive to human amnesia and has been demonstrated to be abnormal in monkeys who have ablation of areas known to produce amnesia in man (e.e., medial temporal lobe and dorsal medial nucleus of the thalamus). We plan to test four groups of monkeys. In one group, the retrosplenial area will be ablated. In the second group, we will ablate only the fornix, near the splenium. In the their group, both areas will be ablated. The fourth group will serve as controls. Use of this delayed non-match task in monkeys with ablation of specific areas can help us understand what specific structures in the splenial region must be damaged to induce amnesia.
