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Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons

Received: 21 February 2018     Accepted: 9 March 2018     Published: 3 April 2018
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Abstract

The aim of the paper was to estimate the effect of experimental cerebral ischemia on metabolic characteristics of parietal cortex neurons. The experiments were carried out on 12 laboratory male rats. Cerebral ischemia was modeled with bilateral joint carotid arteries with durations of 60 minutes under intravenous thiopental anesthesia (40-50 mg / kg). The rats were decapitated and the samples of the brain parietal cortex were prepared for histological and histochemical examination in combination with morphometry to examine the 5th layer inner pyramidal neurons. It was increased the number of pathological forms and shrinkage of the 5th layer inner pyramidal neurons after cerebral ischemia in rats. The histochemical examination was revealed the inhibition of NADH-, glucose-6-phosphate dehydrogenase and succinate dehydrogenases as well as activation of lactate dehydrogenase and acid phosphatase. Cerebral ischemia induces deep histological and histochemical changes in the parietal cortex neurons in rats, including shrinkage of parietal cortex neurons and disturbances of their energy metabolism.

Published in Bioprocess Engineering (Volume 2, Issue 1)
DOI 10.11648/j.be.20180201.11
Page(s) 1-5
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2018. Published by Science Publishing Group

Keywords

Cerebral Ischemia, Parietal Cortex, Neurons

References
[1] Borges N., Cerejo A., Santos A. (2004) Changes in rat cerebral mitochondrial succinate dehydrogenase activity after brain trauma. Int. J. Neurosci., 114, 217–227.
[2] Chalmers G. R., Roy R. R., Edgerton V. R. (1992) Adaptability of the oxidative capacity of motoneurons. Brain. Res., 570, 1–10.
[3] Chan P. H. (2004) Mitochondria and neuronal death/survival signaling pathways in cerebral ischemia. Neurochem. Res., 29, 1943-1949.
[4] Gallyas F (2007) Novel cell-biological ideas deducible from morphological observations on "dark" neurons revisited. Ideggyogy. Sz. 78, 212–222.
[5] Hamilton G. F. (2016) Behavioral deficits induced by third-trimester equivalent alcohol exposure in male C57BL/6J mice are not associated with reduced adult hippocampal neurogenesis but are still rescued with voluntary exercise. Behav Brain Res., 45, 615–620.
[6] Paxinos G & Watson C (2007) The rat brain in stereotaxic coordinates (6th ed). London: Academic Press.
[7] Pearse, A. G. E. (1960). Histochemistry: theoretical and applied (2nd ed). London: Churchill.
[8] Stagliano, NE, Dietrich, WD, Prado, R, Green, EJ, Busto, R (1997) The role of nitric oxide in the pathophysiology of thromboembolic stroke in the rat. Brain Res 759:32–40
[9] Wada, K, Chatzipanteli, K, Busto, R, Dietrich, WD (1998a) The role of nitric oxide in traumatic brain injury in the rat. J Neurosurgery 89:807–818.
[10] Zauner, A, Bullock, R, Kuta, AJ, Woodward, J, Young, HF (1996) Glutamate release and cerebral blood flow after severe human head injury. Acta Neurochir Suppl 6740:6744.
[11] Zhang, F, Sprague, SM, Farrokhi, F, Henry, MN, Son, MG, Vollmer, DG (2002) Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury. J Neurosurg 97:963–969.
[12] White B. C. (2000) Brain ischemia and reperfusion: molecular mechanisms of neuronal injury. J. Neurol. Sci., 176, 1-33.
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    Lizaveta Igorevna Bon, Nataliya Yevgenyevna Maksimovich, Sergey Michailovich Zimatkin. (2018). Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons. Bioprocess Engineering, 2(1), 1-5. https://doi.org/10.11648/j.be.20180201.11

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    ACS Style

    Lizaveta Igorevna Bon; Nataliya Yevgenyevna Maksimovich; Sergey Michailovich Zimatkin. Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons. Bioprocess Eng. 2018, 2(1), 1-5. doi: 10.11648/j.be.20180201.11

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    AMA Style

    Lizaveta Igorevna Bon, Nataliya Yevgenyevna Maksimovich, Sergey Michailovich Zimatkin. Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons. Bioprocess Eng. 2018;2(1):1-5. doi: 10.11648/j.be.20180201.11

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  • @article{10.11648/j.be.20180201.11,
      author = {Lizaveta Igorevna Bon and Nataliya Yevgenyevna Maksimovich and Sergey Michailovich Zimatkin},
      title = {Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons},
      journal = {Bioprocess Engineering},
      volume = {2},
      number = {1},
      pages = {1-5},
      doi = {10.11648/j.be.20180201.11},
      url = {https://doi.org/10.11648/j.be.20180201.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.be.20180201.11},
      abstract = {The aim of the paper was to estimate the effect of experimental cerebral ischemia on metabolic characteristics of parietal cortex neurons. The experiments were carried out on 12 laboratory male rats. Cerebral ischemia was modeled with bilateral joint carotid arteries with durations of 60 minutes under intravenous thiopental anesthesia (40-50 mg / kg). The rats were decapitated and the samples of the brain parietal cortex were prepared for histological and histochemical examination in combination with morphometry to examine the 5th layer inner pyramidal neurons. It was increased the number of pathological forms and shrinkage of the 5th layer inner pyramidal neurons after cerebral ischemia in rats. The histochemical examination was revealed the inhibition of NADH-, glucose-6-phosphate dehydrogenase and succinate dehydrogenases as well as activation of lactate dehydrogenase and acid phosphatase. Cerebral ischemia induces deep histological and histochemical changes in the parietal cortex neurons in rats, including shrinkage of parietal cortex neurons and disturbances of their energy metabolism.},
     year = {2018}
    }
    

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  • TY  - JOUR
    T1  - Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons
    AU  - Lizaveta Igorevna Bon
    AU  - Nataliya Yevgenyevna Maksimovich
    AU  - Sergey Michailovich Zimatkin
    Y1  - 2018/04/03
    PY  - 2018
    N1  - https://doi.org/10.11648/j.be.20180201.11
    DO  - 10.11648/j.be.20180201.11
    T2  - Bioprocess Engineering
    JF  - Bioprocess Engineering
    JO  - Bioprocess Engineering
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    EP  - 5
    PB  - Science Publishing Group
    SN  - 2578-8701
    UR  - https://doi.org/10.11648/j.be.20180201.11
    AB  - The aim of the paper was to estimate the effect of experimental cerebral ischemia on metabolic characteristics of parietal cortex neurons. The experiments were carried out on 12 laboratory male rats. Cerebral ischemia was modeled with bilateral joint carotid arteries with durations of 60 minutes under intravenous thiopental anesthesia (40-50 mg / kg). The rats were decapitated and the samples of the brain parietal cortex were prepared for histological and histochemical examination in combination with morphometry to examine the 5th layer inner pyramidal neurons. It was increased the number of pathological forms and shrinkage of the 5th layer inner pyramidal neurons after cerebral ischemia in rats. The histochemical examination was revealed the inhibition of NADH-, glucose-6-phosphate dehydrogenase and succinate dehydrogenases as well as activation of lactate dehydrogenase and acid phosphatase. Cerebral ischemia induces deep histological and histochemical changes in the parietal cortex neurons in rats, including shrinkage of parietal cortex neurons and disturbances of their energy metabolism.
    VL  - 2
    IS  - 1
    ER  - 

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Author Information
  • Department of Pathological Physiology of the Name of D. A. Maslakov, Grodno State Medical University, Grodno, Belarus

  • Department of Pathological Physiology of the Name of D. A. Maslakov, Grodno State Medical University, Grodno, Belarus

  • Department of Histology, Cytology and Embryology, Grodno State Medical University, Grodno, Belarus

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