Aged monkeys exhibit behavioral deficits indicative of widespread cerebral dysfunction.

To determine whether the decline of behavioral abilities with aging in monkeys is selective or widespread, we examined 18 monkeys ranging from 3 to 34 years of age on a wide variety of tests with the ultimate goal of correlating behavioral deficits with age-related changes in the brain. In our initial study we found impaired visual recognition ability in the aged monkeys (43). In the present study, we assessed the same animals on tests of spatial memory, visual habit formation, visuospatial orientation, visually guided reaching, motor skill learning, and reaction time, these categories having been chosen to test the integrity of different cerebral systems. There were three major findings. First, age-related impairments were observed in nearly all test categories, though often not on easy versions of the tests, suggesting that the deficits observed were in the specific abilities measured and not an artifact of lowered motivation or other general disability. Second, the behavioral decline began in the late teens for certain spatial abilities but did not affect other abilities until the late 20's, suggesting that although the cerebral dysfunction eventually becomes widespread, the cerebral systems underlying spatial abilities are compromised by aging earlier than others. Finally, the finding of correlations between scores of aged animals primarily within test categories as opposed to across categories suggests that different animals have different patterns of cerebral involvement.

Age and sex differences in the effects of selective temporal lobe lesion on the formation of visual discrimination habits in rhesus monkeys (Macaca mulatta).

Three-month-old infant monkeys with neonatal ablations of either cortical area TE or the amygdala and hippocampus and age-matched normal infants were trained in a concurrent object discrimination task with 24-hr intertrial intervals. Neonatal area TE lesions yielded a transient deficit in visual habit formation, present in the female monkeys only, whereas the same lesions in adult monkeys yielded a severe and long-lasting deficit in both males and females. Although pointing to a greater neural compensation for the early loss as compared with the later loss of cortical area TE, the results also corroborate a recent suggestion (Bachevalier, Hagger, & Bercu, 1989) that, at 3 months of age, area TE is more fully functional in females than in males. Neither early nor late amygdalohippocampal lesions impaired the ability to form visual discrimination habits, strengthening the proposal that the habit system uses a corticononlimbic circuit.

Limbic-dependent recognition memory in monkeys develops early in infancy.

Infantile amnesia, the absence of memories from infancy and early childhood, has been attributed to an immaturity of the limbic system in infancy. Contrary to this view, we now report that limbic-dependent recognition memory is present as early as one month of age in monkeys. Memory measured by the paired-comparison preferential looking task, normally present in infant monkeys within the first month of life, is absent after damage to the amygdaloid complex and hippocampal formation, suggesting that limbic structures make a critical contribution to visual recognition memory even at this early age. The findings reopen the question of the locus of the neural immaturity that underlies infantile amnesia.