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53. Biphenyl scaffold for the design of NMDA-receptor negative modulators: molecular modeling, synthesis, and biological activity

Author

Karlov, Dmitry S., primary, Temnyakova, Nadezhda S., additional, Vasilenko, Dmitry A., additional, Barygin, Oleg I., additional, Dron, Mikhail Y., additional, Zhigulin, Arseniy S., additional, Averina, Elena B., additional, Grishin, Yuri K., additional, Grigoriev, Vladimir V., additional, Gabrel'yan, Alexey V., additional, Aniol, Viktor A., additional, Gulyaeva, Natalia V., additional, Osipenko, Sergey V., additional, Kostyukevich, Yury I., additional, Palyulin, Vladimir A., additional, Popov, Petr A., additional, and Fedorov, Maxim V., additional

Published
2022
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59. Identifying the Involvement of Pro-Inflammatory Signal in Hippocampal Gene Expression Changes after Experimental Ischemia: Transcriptome-Wide Analysis

Author

Shishkina, Galina T., primary, Gulyaeva, Natalia V., additional, Lanshakov, Dmitriy A., additional, Kalinina, Tatyana S., additional, Onufriev, Mikhail V., additional, Moiseeva, Yulia V., additional, Sukhareva, Ekaterina V., additional, Babenko, Vladimir N., additional, and Dygalo, Nikolay N., additional

Published
2021
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60. Neuroinflammatory Cytokine Response, Neuronal Death, and Microglial Proliferation in the Hippocampus of Rats During the Early Period After Lateral Fluid Percussion-Induced Traumatic Injury of the Neocortex

Author

Komoltsev, Ilia G., primary, Tret’yakova, Liya V., additional, Frankevich, Stepan O., additional, Shirobokova, Natalia I., additional, Volkova, Aleksandra A., additional, Butuzov, Alexey V., additional, Novikova, Margarita R., additional, Kvichansky, Alexey A., additional, Moiseeva, Yulia V., additional, Onufriev, Mikhail V., additional, Bolshakov, Alexey P., additional, and Gulyaeva, Natalia V., additional

Published
2021
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72. Russian Personal Data Law Amended To Address Publicly Available Data And Fines

Author

Gulyaeva, Natalia

Subjects
Data security -- Laws, regulations and rules, Privacy -- Laws, regulations and rules, Personal information -- Laws, regulations and rules, Government regulation, Data security issue, Privacy issue, Business, international
Abstract

March 2021 brought two significant amendments to Russia's Personal Data Law: one related to processing of publicly available personal data, and another increasing fines for violations of various data privacy [...]

Published
2021

73. Chronic morphine intoxication reduces binding of HuD to BDNF long 3′-UTR, while morphine withdrawal stimulates BDNF expression in the frontal cortex of male Wistar rats

Author

Peregud, Danil, Panchenko, Leonid, and Gulyaeva, Natalia

Subjects
nervous system
Abstract

Brain-derived neurotrophic factor (BDNF) mediates opiate dependence phenomenon. In the brain of morphine dependent animals BDNF level is controlled transcriptionally, however, post-transcriptional mechanisms of BDNF regulation in this context remain unknown. Regulation of mRNA by binding of specific proteins to the 3'-untranslated region (3′-UTR) is one of such mechanisms. Among RNA-binding proteins neuronal Hu antigen D (HuD) is the best characterized positive regulator of BDNF, however its involvement in opiate dependence remains obscure. We suggested that HuD binding to the BDNF 3′-UTR may be linked to changes in BDNF expression induced by morphine. The aim of this study was to investigate potential association of HuD with BDNF 3′-UTR in relation to BDNF expression (Exon- and 3′-UTR-specific mRNA variants and protein level) in the frontal cortex and midbrain of male Wistar rats after chronic morphine intoxication and spontaneous withdrawal in dependent animals. After chronic morphine intoxication but not during morphine withdrawal HuD binding to the long BDNF 3′-UTR in the frontal cortex decreased as compared with the corresponding control group, however after intoxication BDNF expression did not change. The level of BDNF Exon I as well as mature BDNF polypeptide increased in the frontal cortex upon morphine withdrawal, while no changes in HuD binding could be detected. Thus, contrary to the assumption, HuD-BDNF 3′-UTR interaction and BDNF expression in the frontal cortex differentially change in a manner dependent on the context of morphine action.

Published
2020
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77. Chronic morphine intoxication reduces binding of HuD to BDNF long 3′-UTR, while morphine withdrawal stimulates BDNF expression in the frontal cortex of male Wistar rats.

Author

Peregud, Danil, Panchenko, Leonid, and Gulyaeva, Natalia

Subjects
FRONTAL lobe, BRAIN-derived neurotrophic factor, LABORATORY rats, RNA-binding proteins, MORPHINE, BUPRENORPHINE, HEROIN
Abstract

Brain-derived neurotrophic factor (BDNF) mediates opiate dependence phenomenon. In the brain of morphine dependent animals BDNF level is controlled transcriptionally, however, post-transcriptional mechanisms of BDNF regulation in this context remain unknown. Regulation of mRNA by binding of specific proteins to the 3'-untranslated region (3′-UTR) is one of such mechanisms. Among RNA-binding proteins neuronal Hu antigen D (HuD) is the best characterized positive regulator of BDNF, however its involvement in opiate dependence remains obscure. We suggested that HuD binding to the BDNF 3′-UTR may be linked to changes in BDNF expression induced by morphine. The aim of this study was to investigate potential association of HuD with BDNF 3′-UTR in relation to BDNF expression (Exon- and 3′-UTR-specific mRNA variants and protein level) in the frontal cortex and midbrain of male Wistar rats after chronic morphine intoxication and spontaneous withdrawal in dependent animals. After chronic morphine intoxication but not during morphine withdrawal HuD binding to the long BDNF 3′-UTR in the frontal cortex decreased as compared with the corresponding control group, however after intoxication BDNF expression did not change. The level of BDNF Exon I as well as mature BDNF polypeptide increased in the frontal cortex upon morphine withdrawal, while no changes in HuD binding could be detected. Thus, contrary to the assumption, HuD-BDNF 3′-UTR interaction and BDNF expression in the frontal cortex differentially change in a manner dependent on the context of morphine action. [ABSTRACT FROM AUTHOR]

Published
2022
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81. A Translational Study on Acute Traumatic Brain Injury: High Incidence of Epileptiform Activity on Human and Rat Electrocorticograms and Histological Correlates in Rats

Author

Komoltsev, Ilia G., primary, Sinkin, Mikhail V., additional, Volkova, Aleksandra A., additional, Smirnova, Elizaveta A., additional, Novikova, Margarita R., additional, Kordonskaya, Olga O., additional, Talypov, Alexander E., additional, Guekht, Alla B., additional, Krylov, Vladimir V., additional, and Gulyaeva, Natalia V., additional

Published
2020
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93. Biphenyl scaffold for the design of NMDA-receptor negative modulators: molecular modeling, synthesis, and biological activityElectronic supplementary information (ESI) available. See DOI: https://doi.org/10.1039/d2md00001f

Author

Karlov, Dmitry S., Temnyakova, Nadezhda S., Vasilenko, Dmitry A., Barygin, Oleg I., Dron, Mikhail Y., Zhigulin, Arseniy S., Averina, Elena B., Grishin, Yuri K., Grigoriev, Vladimir V., Gabrel'yan, Alexey V., Aniol, Viktor A., Gulyaeva, Natalia V., Osipenko, Sergey V., Kostyukevich, Yury I., Palyulin, Vladimir A., Popov, Petr A., and Fedorov, Maxim V.

Abstract

NMDA (N-methyl-d-aspartate) receptor antagonists are promising tools for the treatment of a wide variety of central nervous system impairments including major depressive disorder. We present here the activity optimization process of a biphenyl-based NMDA negative allosteric modulator (NAM) guided by free energy calculations, which led to a 100 times activity improvement (IC50= 50 nM) compared to a hit compound identified in virtual screening. Preliminary calculation results suggest a low affinity for the human ether-a-go-go-related gene ion channel (hERG), a high affinity for which was earlier one of the main obstacles for the development of first-generation NMDA-receptor negative allosteric modulators. The docking study and the molecular dynamics calculations suggest a completely different binding mode (ifenprodil-like) compared to another biaryl-based NMDA NAM EVT-101.

Published
2022
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95. Glucocorticoid‐mediated mechanisms of hippocampal damage: Contribution of subgranular neurogenesis.

Author

Podgorny, Oleg V. and Gulyaeva, Natalia V.

Subjects
*HIPPOCAMPUS (Brain), *DENTATE gyrus, *MINERALOCORTICOID receptors, *BRAIN diseases, *PROGENITOR cells, *DEVELOPMENTAL neurobiology
Abstract

A comprehensive overview of the interplay between glucocorticoids (GCs) and adult hippocampal neurogenesis (AHN) is presented, particularly, in the context of a diseased brain. The effectors of GCs in the dentate gyrus neurogenic niche of the hippocampal are reviewed, and the consequences of the GC signaling on the generation and integration of new neurons are discussed. Recent findings demonstrating how GC signaling mediates impairments of the AHN in various brain pathologies are overviewed. GC‐mediated effects on the generation and integration of adult‐born neurons in the hippocampal dentate gyrus depend on the nature, severity, and duration of the acting stress factor. GCs realize their effects on the AHN primarily via specific glucocorticoid and mineralocorticoid receptors. Disruption of the reciprocal regulation between the hypothalamic–pituitary–adrenal (HPA) axis and the generation of the adult‐born granular neurons is currently considered to be a key mechanism implicating the AHN into the pathogenesis of numerous brain diseases, including those without a direct hippocampal damage. These alterations vary from reduced proliferation of stem and progenitor cells to increased cell death and abnormalities in morphology, connectivity, and localization of young neurons. Although the involvement of the mutual regulation between the HPA axis and the AHN in the pathogenesis of cognitive deficits and mood impairments is evident, several unresolved critical issues are stated. Understanding the details of GC‐mediated mechanisms involved in the alterations in AHN could enable the identification of molecular targets for ameliorating pathology‐induced imbalance in the HPA axis/AHN mutual regulation to conquer cognitive and psychiatric disturbances. [ABSTRACT FROM AUTHOR]

Published
2021
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100. Cholinergic Deficit Induced by Central Administration of 192IgG-Saporin Is Associated With Activation of Microglia and Cell Loss in the Dorsal Hippocampus of Rats

Author

Dobryakova, Yulia V., primary, Volobueva, Maria N., additional, Manolova, Anna O., additional, Medvedeva, Tatiana M., additional, Kvichansky, Alexey A., additional, Gulyaeva, Natalia V., additional, Markevich, Vlamidir A., additional, Stepanichev, Mikhail Yu., additional, and Bolshakov, Alexey P., additional

Published
2019
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