Numbers of Meynert and layer IVB cells in area V1: A stereologic analysis in young and aged macaque monkeys

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Abstract
Visual impairments that are not related to optical changes are not uncommon during aging, and a number of psychophysical investigations have documented deficits in motion detection as well as in spatiotemporal contrast sensitivity in elderly people. However, little is known about the extent and nature of age‐related changes in neural structure and how they may affect visual function in aging. To address this question, the authors analyzed the effect of aging on two well‐characterized neuronal populations in the primary visual cortex (area V1) of macaque monkeys. Four young adult (ages, 7–11 years) and four aged (ages, 26–32 years) rhesus monkeys were analyzed. The animals were perfused, and their brains were prepared for immunohistochemistry with an antibody to neurofilament protein. Unbiased stereologic estimates of the total numbers of neurofilament protein‐containing layer IVB cells and Meynert cells were obtained by using the optical fractionator method for the calcarine cortex and the opercular cortex separately. Stereologic estimates of the volume of these parts of area V1 also were calculated by using the Cavalieri principle. A considerable degree of interindividual variability in neuron numbers and cortical volume was observed among animals of both groups. However, there were no differences in either Meynert cell numbers or layer IVB cell numbers between the aged group and the young group. It is noteworthy that the oldest animal in the sample had the lowest numbers of Meynert cells, indicating that, despite the small size of the available sample, it is possible that some animals have a certain degree of neuronal loss in area V1 during aging. No change in the volume of area V1 was observed as a function of aging. These data suggest that the deficits that occur during aging in the visual system are not due to the loss of highly specific neocortical neuronal populations, such as those analyzed in this study. Rather, it is possible that more subtle alterations in the neurochemical characteristics or synaptic organization of the functional pathways subserving the different visual modalities are responsible for these deficits. J. Comp. Neurol. 420:113–126, 2000.