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Monkeys with stereotaxic lesions of the amygdaloid complex that spared the surrounding cortex (i.e., the periamygdaloid, entorhinal, and perirhinal cortices) performed normally on the delayed nonmatching to sample task, as well as on 3 other memory tasks (object retention, concurrent discrimination, and delayed response) administered during the 1 1/2 years after surgery. These animals also performed normally on pattern discrimination and motor-skill learning, 2 tasks analogous to ones amnesic patients perform well. A second group of monkeys with conjoint lesions that included both the amygdaloid complex, as just described, and the hippocampal formation were impaired on the same 4 memory tasks. However, the severity of impairment in this group was no greater than in monkeys with lesions of the hippocampal formation alone. Thus, circumscribed bilateral lesions of the amygdala did not impair performance on 4 different memory tasks, nor did they exacerbate the memory impairment that followed hippocampal formation lesions alone. These findings suggest that one must look to structures other than the amygdala to account for the severe memory impairment that follows large lesions of the medial temporal region. One possibility is that damage to the cortical regions that surround the amygdala contributes to memory impairment.

the journal of neuroscience/the journal of neuroscience

Lesions of the amygdala that spare adjacent cortical regions do not impair memory or exacerbate the impairment following lesions of the hippocampal formation