Volume 2, Issue 1, March 2018, Page: 1-5
Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons
Lizaveta Igorevna Bon, Department of Pathological Physiology of the Name of D. A. Maslakov, Grodno State Medical University, Grodno, Belarus
Nataliya Yevgenyevna Maksimovich, Department of Pathological Physiology of the Name of D. A. Maslakov, Grodno State Medical University, Grodno, Belarus
Sergey Michailovich Zimatkin, Department of Histology, Cytology and Embryology, Grodno State Medical University, Grodno, Belarus
Received: Feb. 21, 2018;       Accepted: Mar. 9, 2018;       Published: Apr. 3, 2018
DOI: 10.11648/j.be.20180201.11      View  907      Downloads  30
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.
Keywords
Cerebral Ischemia, Parietal Cortex, Neurons
To cite this article
Lizaveta Igorevna Bon, Nataliya Yevgenyevna Maksimovich, Sergey Michailovich Zimatkin, Effects of Experemental Cerebral Ishemia on Metabolic Characteristics of Parietal Cortex Neurons, Bioprocess Engineering. Vol. 2, No. 1, 2018, pp. 1-5. doi: 10.11648/j.be.20180201.11
Copyright
Copyright © 2018 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Reference
[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.
Browse journals by subject