Acetylcholinesterase in the Cortex

Kristt, Donald A.

doi:10.1007/978-1-4615-6616-8_5

Cited by 9 publications

(1 citation statement)

References 178 publications

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“…22 Some noncholinergic neurons and neuronal fibers may contain acetylcholinesterase. Excitotoxic lesions of the basal forebrain cholinergic neurons, which should not affect other fibers of passage, eliminate a major proportion of acetylcholinesterase-positive fibers in rat neocortex.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic deafferentation after focal cerebral infarct in rats.

Kataoka

Hayakawa

Kuroda

et al. 1991

Stroke

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Background and Purpose: For a better understanding of neuronal network disturbances after stroke, we investigated the changes in the cholinergic system after experimental focal infarct Methods: We quantitatively evaluated the highly sensitive acetylcholinesterase histochemistry and local glucose utilization 7 days after left middle cerebral artery occlusion in Wistar rats.Results: In all rats with occlusion, ihe ipsilateral frontal cortex and the nucleus basalis Meynert developed no infarct, whereas the subcortical striatum did. In the frontal cortex on the occlusion side, the acetylcholinesterase-positive fiber density was significantly (p<0.05) reduced; a computer-assisted image-analyzing system quantified approximately 1.0 m/mm

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Section: Discussionmentioning

confidence: 99%

Cholinergic deafferentation after focal cerebral infarct in rats.

Kataoka

Hayakawa

Kuroda

et al. 1991

Stroke

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Acetylcholinesterase reactivity in the frontal cortex of human and monkey: Contribution of AChE‐rich pyramidal neurons

Mrzljak

Goldman‐Rakic

1992

J of Comparative Neurology

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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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