M. V. Vedunova - Ph.D. (Biol.), Senior Research Scientist, Lobachevsky State University of Nizhni Novgorod, Nizhny Novgorod, Russia. E-mail: MVedunova@yandex.ru
T. A. Sakharnova - Junior Research Scientist, NNSMA, Nizhny Novgorod, Russia. E-mail: saHarnova87@mail.ru
E. V. Mitroshina - Junior Research Scientist, NNSMA, Nizhny Novgorod, Russia. E-mail: Mitroshinae@list.ru
I. V. Mukhina - Dr.Sc. (Biol.), Professor, NNSMA, Nizhny Novgorod, Russia; Lobachevsky State University of Nizhni Novgorod, Nizhny Novgorod, Russia

Nowadays neuroscience and biomedical investigations is focused on an active searching of substances and ways to protect the brain from negative effects of oxygen starvation. Using endogenous neuroprotective substances will potentially minimize the possibility of the development of pathological processes during hypoxia and in the posthypoxic period. Particular attention is directed to studying the mechanisms of action of Brain-derived neurotrophic factor (BDNF) which actively participates not only in the neurogenesis, but can also correct the metabolism of mature neurons. It should be noticed that neuroprotective properties performed by BDNF are determined by its interaction with the tropomyosin-related kinase B (TrkB) receptor, which launches important signaling mechanisms involved in increasing resistance of cells to ischemia damaging factors. However, a question of the certain signaling mechanism of BDNF and the role of TrkB receptor in the regulation of oxidative processes in mature brain remains unclear. The aim of the investigation was to study the role of TrkB receptor on the survival and the main parameters of spontaneous bioelectrical activity of dissociated hippocampal cultures in short-term hypoxia and in the posthypoxic period. Dissociated hippocampal cells were taken from the brain of CBA mice embryos (E18) and cultured during 21 days in vitro (DIV) on multielectrode arrays (Multichannel Systems, Germany). Modeling of hypoxia was performed on 14th DIV by replacing the normoxic culture medium by a medium with low oxygen for 10 minutes. The dynamics of changes in spontaneous bioelectrical activity and the viability of cells were evaluated during 7 days after normobaric hypoxia. The carried out experiments revealed acute normobaric hypoxia to cause irreversible changes in spontaneous bioelectrical activity of dissociated hippocampal cultures and their viability. A preventive application of BDNF (1 ng/ml) reduced negative consequences of the hypoxic injury. Moreover, antihypoxic and neuroprotective properties of BDNF (1 ng/ml) were mainly caused by the activity of the tropomyosin-related kinase B receptor. Application of the selective antagonist of TrkB receptor k252a (150 nM) partially decreased positive effects of preventive using of BDNF (1 ng/ml). Also BDNF prevented the degradation processes of neurons and TrkB on membrane in the posthypoxic period. The research was supported by grants of Russian Foundation of Basic Research № 13-04-01871, № 13-04-12067, № 14-04-31601.