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  • Title: Acetylcholinesterase reactivity in the frontal cortex of human and monkey: contribution of AChE-rich pyramidal neurons.
    Author: Mrzljak L, Goldman-Rakic PS.
    Journal: J Comp Neurol; 1992 Oct 08; 324(2):261-81. PubMed ID: 1430332.
    Abstract:
    Light and electron microscopic histochemistry were used to analyze the distribution of the enzyme acetylcholinesterase (AChE) in the frontal cortex of macaque monkey and human. In prefrontal, premotor, prelimbic, and medial paralimbic areas, AChE reactivity showed a characteristic bilaminar appearance due to a combination of positive neuronal and fiber labeling in deep layer III and layer V. In addition, layer I contained dense AChE-reactive fiber plexuses labeled throughout the frontal areas. One of the major issues addressed in this study was whether pyramidal neurons in the nonhuman primate cortex express AChE reactivity, as has been reported for humans. Three different histochemical methods were applied to provide confidence in the reliability of the results. Light microscopic analysis revealed strongly reactive, intensely stained pyramidal neurons in monkey as well as in the human. Further, these AChE-rich neurons exhibited the same pattern of laminar and regional variation in both species. In the prefrontal and premotor areas, AChE-rich pyramidal neurons predominated in layer III. In the motor cortex, they were also concentrated in layer III, but numerous AChE-rich pyramids were observed in layer V. In contrast, medial paralimbic areas had more AChE-rich neurons in layer V than in layer III. Finally, at the electron microscopic level, the subcellular distribution of AChE histochemical product in pyramidal neurons was identical in both monkey and human. The only difference noted between the two species was that the density of AChE-rich pyramidal neurons was greater in humans than in monkeys. Since nonhuman primates possess a system of AChE-reactive pyramidal neurons similar to human, they provide a potentially useful animal model for analyzing acetylcholinesterase neuronal systems in the cortex, which are compromised in various neuropathological diseases like Alzheimer's disease.
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