T S Glushchenko

Russian Academy of Sciences, Moskva, Moscow, Russia

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Publications (13)0.48 Total impact

  • A V Churilova, T S Glushchenko, M O Samoĭlov
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    ABSTRACT: Hypobaric hypoxia may have either detrimental or adaptive effect on structural and functional characteristics of brain neurons. In this study, the effect of different regimes of hypobaric hypoxia on the structural and functional characteristics of hippocampal and neocortical neurons was examined in rats (n = 30). It was shown that severe hypoxia (induced by pressure in the pressure chamber equal to 180 Torr) caused structural neuronal damage both in the fronto-parietal neocortex and dorsal and ventral hippocampus 3 days after the exposure. The preconditioning using mild hypobaric hypoxia (pressure equal to 360 Torr) had varied effect on the morphological characteristics of brain neurons of rats, subjected to severe hypoxia. Multiple (three-trial or six-trial) preconditioning prevents structural damage of neurons induced by subsequent severe hypoxia. On the contrary, single preconditioning trial of mild hypoxia was ineffective in terms of neuroprotection.
    Morfologiia (Saint Petersburg, Russia) 01/2012; 141(1):7-11.
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    ABSTRACT: Preconditioning using three sessions of moderate hypobaric hypoxia, i.e., hypoxic preconditioning (HP), increased the tolerance of susceptible brain neurons to severe hypoxia and other harmful factors. The study addressed changes in the expression of transcription factors NF-kappaB (nuclear factor kappa B) and CREB (cAMP response element binding protein) in the hippocampus of rats preconditioned with moderate hypoxia. Immunocytochemical methods demonstrated that HP increased immunoreactivity for NF-kappaB and phosphorylated CREB (pCREB) in hippocampal fields CA1-CA4 and the dentate gyrus and promoted increases in the expression of these transcription factors in the hippocampus of preconditioned rats 3-24 h after severe hypobaric hypoxia. These data provide evidence that NF-kappaB and CREB are involved in the mechanisms forming HP-induced tolerance of the brain.
    Neuroscience and Behavioral Physiology 10/2010; 40(8):852-7.
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    ABSTRACT: Previous studies have demonstrated that preconditioning (PC) with three sessions of moderate hypoxia significantly increases the expression of the antioxidant protein thioredoxin-1 (Trx-1) in the rat hippocampus by 3 h after subsequent acute severe hypoxia as compared with non-preconditioned animals. However, it remained unclear whether this increase in Trx-1 accumulation during PC is induced before severe hypoxia or is a modification of the response to severe hypoxia. This question was addressed in the present investigation using experiments on 12 adult male Wistar rats with studies of Trx-1 expression after PC without subsequent severe hypoxia. Immunocytochemical studies were performed 3 and 24 h after three episodes of moderate hypobaric hypoxia (three sessions of 2 h at 360 mmHg with 24-h intervals). Immunoreactivity to Trx-1 24 h after the last session was significantly decreased in neurons in all the areas of the hippocampus studied (CA1, CA2, CA3, and the dentate gyrus). Immunoreactivity in CA3 was also decreased 3 h after hypoxia. These results provide evidence that moderate preconditioning hypoxia itself not only does not increase, but even significantly decreases Trx-1 expression. Thus, increases in Trx-1 contents in the hippocampus of preconditioned animals after severe hypoxia are not associated with the accumulation of this protein during PC, but with a PC-induced modification of the reaction to severe hypoxia.
    Neuroscience and Behavioral Physiology 01/2009; 39(1):1-5.
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    ABSTRACT: The effect of preconditioning by a moderate hypobaric hypoxia on changes in the activity of the mitogen-activated (MAP) kinases EPK, JNK 1/2, and p38 and the c-Jun transcriptional factor in rat hippocampus in response to the severe hypoxia was studied using the methods of quantitative immunocytochemistry and Western-blot analysis. Severe damaging hypoxia caused a persistent activation of the JNK cascade, including JNK 1/2 and c-Jun, and also p38 kinase in the hippocampus cells. The preconditioning efficiently inhibited the expression of phosphorylated forms of JNK, c-Jun, and p38 and activated the protein kinase ERK following the severe hypoxia, which obviously promoted the survival of hippocampal neurons. The results indicate the important role of the family of MAP kinases and the c-Jun transcription factor in the processes of neuronal death/survival of the hippocampal neurons after a severe hypobaric hypoxia, and a correcting effect of preconditioning action.
    Neurochemical Journal 09/2007; 1(3):219-226. · 0.24 Impact Factor
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    ABSTRACT: The Nissl method and immunocytochemistry were used to study the effects of severe hypobaric hypoxia and its actions in combination with the preconditioning actions of moderate hypoxia on the expression of the early gene proteins c-Fos and NGFI-A as well as structural changes in hippocampal and neocortical neurons in the rat brain. Severe hypoxia was found to suppress c-Fos and NGFI-A synthesis (3-24 h after exposure) and to induce delayed (days 3-7) structural damage to neurons, of the "light" and predominantly the "dark" types, which appear to reflect the development of necrotic and apoptotic processes respectively. Preconditioning with the regime used here corrected these derangements, resulting in increases in the expression of early gene proteins and significant reductions in structural damage to neurons after severe hypoxia.
    Neuroscience and Behavioral Physiology 06/2005; 35(4):383-8.
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    ABSTRACT: The effects of severe hypobaric hypoxia and preconditioned severe hypoxia on the expression of early genes products--proteins c-Fos and NGFI-A, and structural changes in rat hippocampal and neocortical neurons were studied using Nissl staining and immunocytochemistry. Severe hypoxia was found to induce a suppression of c-Fos and NGFI-A synthesis (at 3-24 h after exposure) and delayed (by day 3-7) destructive neuronal changes, which developed according to "light" and predominantly "dark" type, that obviously reflected necrotic or apoptotic processes, respectively. The preconditioning in the regime applied abolished these pathological changes, as expressed by stimulation of early gene products expression and marked reduction of neuronal damage following severe hypoxia.
    Morfologiia (Saint Petersburg, Russia) 02/2004; 125(2):10-5.
  • T S Glushchenko, L N Grinkevich
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    ABSTRACT: Levels of the acidic brain-specific Rf = 0.58 protein in neurons of the subglottal complex of ganglia were studied in the common snail during the process of acquisition of defensive food aversion. Levels were significantly increased in neurons LPa3 and RPa3 at both the early and late stages of learning. There was a tendency to increased protein levels in neurons LP11 and RP12, while there were no changes in levels in neuron RPa5 and pool D. The level of involvement of defensive behavior command neurons appears to be determined by the specific involvement of their receptor and effector fields.
    Neuroscience and Behavioral Physiology 02/2003; 33(1):49-52.
  • T S Glushchenko, L N Grinkevich
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    ABSTRACT: At early stages of aversive conditioning in Helix, a most considerable increase in the acid brain-specific protein Rf 0.58 occurred in LPa3 and PPa3 neurones. Later the content of this protein decreased in the PPa3 but went on increasing in LPa3. In sham learning, the protein content did not increase so obviously. Hence the protein Rf 0.58 metabolism in individual neurones of the snail CNS correlates with the draw step of receptor and effector fields in avoidance conditioning.
    Rossiĭskii fiziologicheskiĭ zhurnal imeni I.M. Sechenova / Rossiĭskaia akademiia nauk 07/2001; 87(6):774-8.
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    ABSTRACT: A 2-week neurotization of two rat lines formed a long-term stress and increased neuronal Na+,K(+)-ATPase activity in hippocampus, locus coeruleus and n. raphe dorsalis, whereas the glial enzyme activity was decreased in hippocampus and N. raphe dorsalis. (Line H). In rats with low threshold of excitability (line L), the decrease of the Na+,K(+)-ATPase activity occurred in n. raphe dorsalis and hippocampus. After a 15-day rest, the activity decreased in all the structures of the line rats, whereas in the line L rats the activity was still increased in hippocampal neurons. Differences between the rat lines and dependence of the enzyme activity on the functional state of the nervous system, are discussed.
    Fiziologicheskiĭ zhurnal SSSR imeni I. M. Sechenova 03/1992; 78(2):1-7.
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    ABSTRACT: The influence was studied of 15-days stressing on the appearance of stable neurosis-like state of rats lines, selected by the excitability of the nervous system. Unconditioned and conditioned components of behaviour were tested: pain sensitivity, behaviour in the open field, level of "anxiety", passive and active defensive avoidance. Differential reactivity was shown of the rats lines to prolonged stressing, depending on the genetically determined level of the nervous system functional state. Interlinear differences in dynamics of the development of neurosis-like state were established.
    Zhurnal vysshei nervnoi deiatelnosti imeni I P Pavlova 01/1992; 42(1):137-43. · 0.25 Impact Factor
  • T S Glushchenko, D A Kulagin, N G Lopatina, L Z Pevzner
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    ABSTRACT: A single session of the food conditioning in rats entailed an increase of labelled phenylalanine incorporation into the proteins of the nuclei and, particularly, of the cytoplasm of CA3 hippocampal neurons. In the trained animals, as compared with active control group, a session repeated in 3 days returned the turnover of neuronal proteins to the control level, while the same session in 6 days of decreased the protein turnover below the control level. No changes occurred in the course of the experiment in the perineuronal neuroglial cells. Predominant involvement of neuronal protein metabolism is outlined in the metabolic reconstruction within the whole neuron-neuroglia unit in the course of conditioning.
    Fiziologicheskiĭ zhurnal SSSR imeni I. M. Sechenova 11/1978; 64(10):1386-90.
  • Doklady Akademii nauk SSSR 01/1974; 213(6):1458-60.
  • Doklady Akademii nauk SSSR 221(1):243-6.