Open AccessSTUDY OF Na/K-ATPhase α-SUBUNIT DISTRIBUTION IN RAT CEREBRAL STRUCTURES IN PARKINSON-LIKE SYNDROME MODEL AND AFTER THYMUS HORMONE CORRECTION
Author(s) -
Anatoliy Korolev,
А. В. Новоселецкая,
Н. М. Киселева
Publication year - 2020
Publication title -
rossijskij immunologičeskij žurnal/russian journal of immunology
Language(s) - English
Resource type - Journals
eISSN - 2782-7291
pISSN - 1028-7221
DOI - 10.46235/1028-7221-004-son
Subject(s) - mptp , medicine , endocrinology , striatum , prefrontal cortex , neurotoxin , parkinson's disease , cerebral cortex , gene isoform , hormone , cerebellum , protein subunit , hippocampus , chemistry , hypothalamus , dopamine , biology , neuroscience , disease , biochemistry , cognition , gene
Here we examined distribution of Na/K-ATPhase α-subunit in rat cerebral structures, which activity changes in Parkinson-like syndrome. The study was aimed at analyzing quantitative change in diverse different isoforms of Na/K-ATPhase α-subunit in model of Parkinson-like syndrome as well as after refining it by using thymus hormone thymulin. The study was performed on 42 sixweek-old Wistar rats males by dividing animals into 3 groups: 2 experimental and 1 control group. To simulate Parkinson-like syndrome, a solution of 1-methyl 4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) was administered intranasally. 10 days after MPTP inoculation, thymus hormone thymulin was abdominally administered to animals in one experimental group for 5 days. It was demonstrated that level of tissue-specific isoforms of Na/K-ATPhase α-subunit was peaked in hypothalamus, amygdaloid body and striatum, the minimal level was observed in medial prefrontal and prefrontal cortex. It was estimated that in MPTP-stimulated model of Parkinson’s disease, the level of Na/K-ATPhase α1-subunit was significantly higher in striatum, amount of α2-subunits was decreased in the hippocampus, whereas the level of α3-subunit was elevated in the cerebellum compared to control group. Administration of thymus hormone thymulin corrected changes in level of α1, α2 and α3-subunits observed after exposure to neurotoxin.