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Apoptotic and necrotic cell death following kindling induced seizures

S Pretel1, C D Applegate, D Piekut

  • 1Department of Neurobiology and Anatomy, School of Medicine and Dentistry, Rochester, N.Y. 14641, USA.

Acta Histochemica
|March 1, 1997
PubMed

Insights

Kindling-induced seizures cause both hippocampal and extrahippocampal neuron death via apoptosis and necrosis. Diseased neurons express somatostatin or the NMDA receptor (NMDAR1).

Area of Science:

  • Neuroscience
  • Cell Biology
  • Epilepsy Research

Background:

  • Epilepsy is characterized by recurrent seizures, which can lead to neuronal damage.
  • The specific mechanisms and cell types affected by kindling-induced seizures require further elucidation.

Purpose of the Study:

  • To investigate the types of cell death (apoptosis vs. necrosis) occurring in neurons after kindling-induced seizures.
  • To identify which specific neuronal populations undergo cell death and their molecular markers.

Main Methods:

  • Seizures were induced in rats via kindling from the entorhinal cortex.
  • TUNEL and silver impregnation techniques were employed to differentiate apoptotic and necrotic cell death.
  • Immunocytochemistry was used to detect somatostatin and NMDA receptor (NMDAR1) expression in affected neurons.

Main Results:

  • Kindling-induced seizures resulted in the death of both hippocampal and extrahippocampal neurons.
  • Both apoptotic and necrotic cell death pathways were observed in the diseased neurons.
  • A subset of dying neurons expressed somatostatin, while others expressed the NMDAR1, with both types found in hippocampal and extrahippocampal regions.

Conclusions:

  • Kindling-induced seizures trigger diverse neuronal death mechanisms and affect widespread neuronal populations.
  • The expression of somatostatin and NMDAR1 in dying neurons suggests their involvement in seizure-related pathology.
  • Understanding these cell death pathways and neuronal markers is crucial for developing targeted epilepsy therapies.

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