Affiliation:
1. Kazan Federal University
2. Arbuzov Institute of Organic and Physical Chemistry, FRC Kazan Scientific Center, Russian Academy of Sciences
Abstract
A model of pharmacological paralysis in the hind limbs of CD-1 mice was introduced. In the initial phase (before paralysis), the activity of MAO-A, a key enzyme of neuroamine metabolism, was inhibited, leading to increased levels of steroid hormones and prolactin, as well as to a decrease in hepatic CYP3A4 and CYP2D6 activities and astrocytic S-100 protein secretion into the blood serum. In the second phase (paralysis manifestation), the mice exhibited hind limb paralysis development, accumulation of cortisol granules, destruction of capillaries, and aggregation of deformed red blood cells in the cerebral cortex and hippocampal regions.
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