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  • Title: Neuronal organization and plasticity in adult monkey visual cortex: immunoreactivity for microtubule-associated protein 2.
    Author: Hendry SH, Bhandari MA.
    Journal: Vis Neurosci; 1992 Nov; 9(5):445-59. PubMed ID: 1333277.
    Abstract:
    Immunocytochemical staining for microtubule-associated protein 2 (MAP 2) was used to examine the morphology of neurons, the organization of neuronal groups, and the neurochemical plasticity of cells in adult monkey area 17. MAP 2-immunostained neurons are present through the depth of area 17 but are most intensely immunoreactive in layers IVB and VI. From layer IVB, separate groups of MAP 2-positive cells invade layers IVA and IVC alpha. Clusters of cells protrude upward from superficial layer IVB and occupy the central core regions of the cytochrome oxidase (CO)-stained honeycomb in layer IVA, while large neurons typical of layer IVB are distributed in irregular clusters in the subjacent layer IVC alpha. The somata in the layer IVA honeycomb cores give off immunostained dendrites which remain largely within the core regions. Patches of MAP 2-positive neurons are also present in layers II and III, where they coincide with the CO-stained puffs. Intravitreal injections of tetrodotoxin (TTX) into one eye of adult monkeys produce stripes of alternating light and dark MAP 2 immunostaining in layer IVC. Stripes of light immunostaining coincide with stripes of light CO staining, and correspond to reduced MAP 2 immunoreactivity within cortical neurons dominated by the TTX-injected eye. In layers II and III, the MAP 2 immunostaining of patches overlying the injected-eye columns is similarly reduced. No change occurs in the MAP 2 immunostaining of layer IVA. These data suggest that the anatomical and physiological heterogeneity of layers IVA and IVC alpha arises from the periodic invasion of neurons characteristic of layer IVB, that the neurons in layer IVA have dendrites confined to thalamocortical-recipient or nonrecipient zones and that the expression of MAP 2 changes in adult cortical neurons following the loss of retinal input.
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