THE ULTRASTRUCTURE OF HIPPOCAMPALCA1 AREA OF THE RAT AFTER STATUS EPILEPTICUS PROVOKED BY KAINIC ACID SYSTEMIC ADMINISTRATION



Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

The ultrastructure of hippocampal CA1 area was investigated in rats 14 days after status epilepticus was induced by kainic acid. The structural alterations were found in 40% of the cells, predominantly in interneurons, which demonstrated both reversible changes (mitochondria with a dilated space between cristae and electron-dense matrix or mitochondria with few short cristae and moderately widened rough endoplasmic reticulum [RER] cisterns with few ribosomes) and more significant alterations (swollen mitochondria containing single dilapidated cristae, including those with damaged mitochondraial membranes, pathologically dilated RER profiles and focal or peripheral chromatolysis. In the areas subjected to chromatolysis, the membrane-like inclusions and vacuoles were sometimes observed. Besides, large osmiophilic irregular structures, surrounded by astrocyte processes rich in glycogen granules and gliofibrills, were rarely found in the neuropil. The synaptic architectonics was also changed. Asymmetrical synapses on small dendrites and spines containing osmiophilic postsynaptic zone were frequently observed. Their synaptic endings contained numerous synaptic vesicles and large vesicles with a central dense core. Some part of presynaptic endings showed clear signs of a classical dark-type degeneration. As in all the altered neurons the nucleus remained intact, we suggest that after status epilepticus the majority of the cells underwent the necrotic-type pathological changes.

About the authors

N T Kotariya

T Z Bikashvili

M G Zhvaniya

Ts G Chkhikvishvili

N T Kotaria

I. Beritashvili Institute of Physiology

; I. Beritashvili Institute of Physiology

T Z Bikashvili

I. Beritashvili Institute of Physiology

; I. Beritashvili Institute of Physiology

M G Zhvania

I. Beritashvili Institute of Physiology

; I. Beritashvili Institute of Physiology

T G Chkhikvishvili

I. Beritashvili Institute of Physiology

; I. Beritashvili Institute of Physiology

References

  1. Боголепов Н.Н. Ультраструктура мозга при гипоксии. М., Медицина, 1979.
  2. Ben-Ari Y. and Cossart R. Kainate, a double agent that generates seizures: two decades of progress. Trends Neurosci., 2000, v. 23, p. 580-587.
  3. Charriaut-Marlangue C. and Ben-Ari Y.A. Cautionary note on the use of the TUNEL stain to determine apoptosis. NeuroReport, 1995, v. 7, № 1, p. 61-67.
  4. Doonan F. and Cotter T.G. Morphological assessment of apoptosis. Methods, 2008, v. 44, № 3, p. 200-204.
  5. Fujikawa D.G., Shinmei S.S. and Cai B. Kainic acid - induced seizures produce necrotic, not apoptotic neurons with internucleosomal DNA cleavage: implications for programmed cell death mechanisms. Neuroscience, 2000, v. 98, № 1, p. 41-53.
  6. Heinemann U., Bucheim K., Gabriel S. et al. Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus. Prog. Brain Res., 2002, v. 135, p. 197-200.
  7. Jiang W., Du B., Chi Z. et al. Preliminary explorations of the role of mitochondrial proteins in refractory epilepsy: some findings from comparative proteomics. J. Neurosci. Res., 2007, v. 85, № 14, p. 3160-1170.
  8. Kotaria N.T., Bolkvadze T., Chkhikhvisvili C.L. et al. Quantitative analysis of cells in rat hippocampus at different time-points after status epilepticus induced by kainic acid administration. Georgian J. Neurosc., 2006, v. 1, № 5, p. 47-52.
  9. Kunz W.S., Kadin A.P., Vielbaher S. et al. Mitochondrial complex 1 deficiency in the epileptic focus of patients with temporal lobe epilepsy. Ann. Neurol., 2000, v. 48, p. 766-773.
  10. Leite J.P., Neder L., Arisi G.M. et al. Plasticity, synaptic strength, and epilepsy: what can we learn from ultrastructural data? Epilepsia. 2005, v. 6 Suppl. 5, p. 134-141.
  11. Mikati M.A., Abi-Habib R.J., El Sabban M.E. et al. Hippocampal programmed cell death after status epilepticus: evidence for NMDA receptor and ceramide mediated mechanism. Epilepsia, 2003, v. 44, p. 282-291.
  12. Pollard H., Charriaut-Marlangue C., Cantagrel S. et al. Kainate acid-induced apoptotic cell death in hippocampal neurons. Neuroscience, 1994, v. 63, p. 7-18.
  13. Walter C., Murphy B.L., Pun R.Y. et al. Pilocarpine-induced seizures cause selective time-dependent changes to adult-generated hippocampal dentate granule cells. J. Neurosci., 2007, v. 27, № 28, p. 7541-7552.
  14. Yao-Chung Chuang, Alice Y.W., Jui-Wei Lin et al. Mitochondrial dysfunction and ultrastructural damage in the hippocampus during kainic acid-induced status epilepticus in the rat. Epilepsia, 2004, v. 45, № 10, p. 1202-1209.
  15. Zhivotosky B. and Orrenius S. Assessment of apoptosis and necrosis by DNA fragmentation and morphological criteria. Curr. Protoc. Cell Biol., 2001, Chapter 18, Unit 18.3, p. 207-221.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2009 Eco-Vector


СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: № 0110212 от 08.02.1993.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies