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Effects of L-alpha-aminoadipic acid on neurons and glia of the rat brain striatum
Author(s) -
Д. Н. Воронков,
Р. М. Худоерков,
Yu. V. Dikalova,
A. V. Stavrovskaya,
A.S. Guschina,
A. S. Ol’shanskiy
Publication year - 2021
Publication title -
kliničeskaâ i èksperimentalʹnaâ morfologiâ
Language(s) - English
Resource type - Journals
eISSN - 2686-6749
pISSN - 2226-5988
DOI - 10.31088/cem2021.10.3.65-73
Subject(s) - astrocyte , striatum , microglia , glutamine synthetase , glial fibrillary acidic protein , gliosis , neun , glutamine , biology , neuroglia , microbiology and biotechnology , neuron , glutamate receptor , neuroscience , chemistry , biochemistry , amino acid , central nervous system , immunohistochemistry , immunology , inflammation , receptor , dopamine
. Few published studies have examined the role of glia-neuron interactions in neurodegen-eration. In this regard, the search for new experimental models is important. L-alpha-aminoadipic acid (L-AA), being a structural analogue of glutamate with a selective toxic effect on astroglia, is of particular interest. However, morphological and neurochemical changes caused by L-AA still remain unclear. The aim of the study was to characterize immunomorphological changes of glia and neurons in the striata of rats after L-AA administration. Materials and methods. On days 3 and 12 after L-AA stereotaxic administration, we studied astrocytic pro-teins localization using immunofluorescence methods: GFAP, vimentin, glutamine synthetase, along with oligodendroglia (by cyclonucleotidphosphatase expression), microglia (IBA1 Ca-binding protein), neuronal nuclear protein NeuN, and the astroglia proliferative activity (based on Ki67 localization). Results. We detected astrocyte death and a decrease in glutamine synthetase immunoreactivity in the le-sioned area, but no changes in the microglia reaction and the L-AA effect on neurons and oligodendroglia. The astrocyte loss was replenished by proliferation and migration of newly formed immature astrocytes, and a glial scar formed on day 12 after the surgery. Conclusion. L-AA administration, which causes the death of striatum astrocytes in the injection area, can serve as a convenient model for studying reactive changes in astroglia and astrocytic dysfunction while revealing the pathogenetic patterns of neurodegenerative processes. Keywords: astrocytes, striatum, L-alpha-aminoadipic acid, gliosis, glial toxin

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