Skip to main content
Log in

Ultrastructure of Hippocampal Field CA1 in Rats after Status Epilepticus Induced by Systemic Administration of Kainic Acid

  • Published:
Neuroscience and Behavioral Physiology Aims and scope Submit manuscript

The ultrastructure of hippocampal field CA1 in rats was studied 14 days after status epilepticus induced by administration of kainic acid. Structural changes were seen in 40% of cells, predominantly interneurons, which showed both reversible changes (mitochondria with an electron-dense matrix or small numbers of short cristae, moderate dilation of rough endoplasmic reticulum (RER) cisterns, and small numbers of ribosomes) and more significant abnormalities: swollen mitochondria with very small numbers of cristae, which were partially degraded, some with damaged mitochondrial membranes, along with pathologically damaged RER components and focal or peripheral chromatolysis. Chromatolyzed areas sometimes contained membrane-like includes and vacuoles. In addition, the neuropil contained occasional large osmiophilic formations surrounded by astrocyte processes with accumulations of glycogen or gliofibrils. Synaptoarchitectonics were also altered. Asymmetrical synapses were often seen on small dendrites and spines, with highly osmiophilic postsynaptic zones, their synaptic terminals containing numerous synaptic vesicles and large vesicles with electron-dense cores. Some presynaptic endings showed clear signs of classical dark-type degeneration. As the nucleus remained intact in all types of altered neurons, it appears that most cells underwent pathological changes of the necrotic type.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. N. N. Bogolepov, Brain Ultrastructure in Hypoxia [in Russian], Meditsina, Moscow (1979).

    Google Scholar 

  2. Y. Ben-Ari and R. Cossart, “Kainate, a double agent that generates seizures: two decades of progress,” Trends Neurosci., 23, 580–587 (2000).

    Article  CAS  PubMed  Google Scholar 

  3. C. Charriaut-Marlangue and Y. Ben-Ari, “A cautionary note on the use of the TUNEL stain to determine apoptosis,” NeuroReport, 7, No. 1, 61–67 (1995).

    CAS  PubMed  Google Scholar 

  4. F. Doonan and T. G. Cotter, “Morphological assessment of apoptosis,” Methods, 44, No. 3, 200–204 (2008).

    Article  CAS  PubMed  Google Scholar 

  5. D. G. Fujikawa, S. S. Shinmei, and B. Cai, “Kainic acid-induced seizures produce necrotic, not apoptotic neurons with internucleosomal DNA cleavage: implications for programmed cell death mechanisms,” Neurosci., 98, No. 1, 41–53 (2000).

    Article  CAS  Google Scholar 

  6. U. Heinemann, K. Bucheim, S. Gabriel, et al., “Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus,” Prog. Brain Res., 135, 197–200 (2002).

    Article  CAS  PubMed  Google Scholar 

  7. W. Jiang, B. Du, Z. Chi, et al., “Preliminary explorations of the role of mitochondrial proteins in refractory epilepsy: some findings from comparative genomics,” J. Neurosci. Res., 85, No. 14, 3160–3170 (2007).

    Article  CAS  PubMed  Google Scholar 

  8. N. T. Kotaria, T. Bolkvadze, C. L. Chkhikhvisvili, et al., “Quantitative analysis of cells in rat hippocampus at different time-points after status epilepticus induced by kainic acid administration,” Georgian J. Neurosci., 1, No. 5, 47–52 (2006).

    Google Scholar 

  9. W. S. Kunz, A. P. Kadin, S. Vielbaher, et al., “Mitochondrial complex 1 deficiency in the epileptic focus of patients with temporal lobe epilepsy,” Ann. Neurol., 48, 766–773 (2000).

    Article  CAS  PubMed  Google Scholar 

  10. J. P. Leite, L. Neder, G. M. Arisi, et al., “Plasticity, synaptic strength, and epilepsy: what can we learn from ultrastructural data?” Epilepsia, 6, Supplement 5, 134–141 (2005).

    Article  Google Scholar 

  11. M. A. Mikati, R. J. Abi-Habib, M. E. Sabban, et al., “Hippocampal programmed cell death after status epilepticus: evidence for NMDA receptor and ceramide mediated mechanism,” Epilepsia, 44, 282–291 (2003).

    Article  CAS  PubMed  Google Scholar 

  12. H. Pollard, C. Charriaut-Marlangue, S. Cantagrel, et al., “Kainate acid-induced apoptotic cell death in hippocampal neurons,” Neurosci., 63, 7–18 (1994).

    Article  CAS  Google Scholar 

  13. C. Walter, B. L. Murphy, R. Y. Pun, et al., “Pilocarpine-induced seizures cause selective time-dependent changes to adult-generated hippocampal dentate granule cells,” J. Neurosci., 27, No. 28, 7541–7552 (2007).

    Article  CAS  PubMed  Google Scholar 

  14. Yao-Chung Chuang,Y. W. Alice, Jui-Wei Lin, et al., “Mitochondrial dysfunction and ultrastructural damage in the hippocampus during kainic acid-induced status epilepticus in the rat,” Epilepsia, 45, No. 10, 1202–1209 (2004).

    Article  PubMed  Google Scholar 

  15. B. Zhivotosky and S. Orrenius, “Assessment of apoptosis and necrosis by DNA fragmentation and morphological criteria,” in: Curr. Protoc. Cell Biol., Chapter 18, Unit 18.3, pp. 207–221.

Download references

Author information

Authors and Affiliations

Authors

Additional information

Translated from Morfologiya, Vol. 135, No. 1, pp. 17–20, January–February, 2009.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Kotariya, N.T., Bikashvili, T.Z., Zhvaniya, M.G. et al. Ultrastructure of Hippocampal Field CA1 in Rats after Status Epilepticus Induced by Systemic Administration of Kainic Acid. Neurosci Behav Physi 40, 127–130 (2010). https://doi.org/10.1007/s11055-009-9233-4

Download citation

  • Received:

  • Revised:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11055-009-9233-4

Key words

Navigation