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Mikhail Stepanichev

Researcher at Russian Academy of Sciences

Publications -  40
Citations -  801

Mikhail Stepanichev is an academic researcher from Russian Academy of Sciences. The author has contributed to research in topics: Hippocampus & Cholinergic neuron. The author has an hindex of 15, co-authored 38 publications receiving 673 citations.

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Amyloid-beta(25-35)-induced memory impairments correlate with cell loss in rat hippocampus.

TL;DR: A gradually developing oxidative stress was evident in the hippocampus of rats treated with Abeta(25-35) as indicated by the increase in 2-thiobarbituric acid (TBARS) reactive substances and superoxide generation, suggesting the involvement of oxidative stress in Abeta-induced neurodegeneration and a relation between memory impairment and neurodegenersation in the CA1 subfield of the hippocampus.
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Rodent Models of Depression: Neurotrophic and Neuroinflammatory Biomarkers

TL;DR: The present review focuses on the numerous experimental rodent models of depression induced by different stress factors during early life (including prenatal period) or adulthood, giving emphasis to the data on the changes of neurotrophic factors and neuroinflammatory indices in the brain.
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Amyloid-β (25–35) increases activity of neuronal NO-synthase in rat brain

TL;DR: It is hypothesized that increased synthesis of NO induced by A beta(25-35) is related to qualitative alterations of nNOS molecule, but not to changes in NOS protein expression, as well as the mechanisms of neurodegenerative diseases including Alzheimer's disease.
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Neonatal proinflammatory challenge in male Wistar rats: Effects on behavior, synaptic plasticity, and adrenocortical stress response.

TL;DR: In this paper, the effects of neonatal proinflammatory stress on the development of anxiety and depressive-like behavior, stress responsiveness, hippocampal plasticity and conditioned fear response were studied in adolescent and adult male Wistar rats.
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Effects of tumor necrosis factor-alpha central administration on hippocampal damage in rat induced by amyloid beta-peptide (25-35).

TL;DR: Surprisingly, administration of TNFα into the cerebral ventricles prevented this Aβ(25–35)‐induced increase in hippocampal caspase‐3 activity, and the results are discussed from the perspective of dual (neuroprotective and neurodestructive) roles of T NF in the brain.