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Natalya P. Bondar

Researcher at Russian Academy of Sciences

Publications -  20
Citations -  383

Natalya P. Bondar is an academic researcher from Russian Academy of Sciences. The author has contributed to research in topics: Social defeat & Midbrain Raphe Nuclei. The author has an hindex of 10, co-authored 20 publications receiving 296 citations. Previous affiliations of Natalya P. Bondar include Novosibirsk State University.

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Effects of Early-Life Stress on Social and Anxiety-Like Behaviors in Adult Mice: Sex-Specific Effects.

TL;DR: The hypothesis that brief separation of pups from their mothers (handling), which can be considered as moderate stress, may result in future positive changes in behavior is supported.
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Downregulation of Serotonergic Gene Expression in the Raphe Nuclei of the Midbrain Under Chronic Social Defeat Stress in Male Mice

TL;DR: It has been shown that mRNA levels of the Tph2, Maoa, Sert, Htr1a, Bdnf, and Creb genes in the raphe nuclei of defeated mice are decreased as compared with the controls, and period of relative rest is not enough for most serotonergic genes to recover expression to the control levels.
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Brain-derived neurotrophic factor and early-life stress: Multifaceted interplay.

TL;DR: This mini-review focuses on the structure and regulation of the Bbnf gene as well as on the stress–BDNF interactions under early-life adverse conditions.
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Altered Hippocampal Neurogenesis and Amygdalar Neuronal Activity in Adult Mice with Repeated Experience of Aggression

TL;DR: The results indicate that extended positive fighting experience in a social conflict heightens aggression, increases proliferation of neuronal progenitors and production of young neurons in the hippocampus, and decreases neuronal activity in the amygdala; these changes can be modified by depriving winners of the opportunity for further fights.
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Molecular Adaptations to Social Defeat Stress and Induced Depression in Mice

TL;DR: The data show that the development of depression under social stress conditions is correlated with suppression of the overactive molecular response to induced stress, involving gene regulatory resistance to glucocorticoid molecules, potentially via a chromatin remodeling mechanism.