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Network Analysis of Foramen Ovale Electrode Recordings in Drug-resistant Temporal Lobe Epilepsy Patients
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Published on: December 18, 2016

The role of synaptic reorganization in mesial temporal lobe epilepsy

Jose E Cavazos1, Devin J Cross

  • 1South Texas Comprehensive Epilepsy Center and Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. cavazosj@uthscsa.edu

Epilepsy & Behavior : E&B
|February 28, 2006
PubMed

Insights

Mechanisms of mesial temporal lobe epilepsy (MTLE) are unclear. New research shows CA1 pyramidal axon plasticity in the hippocampus may cause widespread hyperexcitability and intractable seizures in MTLE.

Area of Science:

  • Neuroscience
  • Epileptology
  • Cellular and Molecular Biology

Background:

  • Mesial temporal lobe epilepsy (MTLE) mechanisms remain uncertain, despite characteristic clinical and neurophysiological findings.
  • Mossy fiber pathway reorganization is a known factor increasing hippocampal network excitability.
  • Plasticity beyond the mossy fiber pathway requires further investigation.

Purpose of the Study:

  • To investigate morphological plasticity of CA1 pyramidal axons in experimental models of MTLE.
  • To elucidate novel mechanisms contributing to hippocampal hyperexcitability in MTLE.

Main Methods:

  • Utilized acute and chronic experimental models of MTLE.
  • Examined plasticity of CA1 pyramidal axons and their projections to the subiculum.

Main Results:

  • Demonstrated plasticity of CA1 pyramidal axons in experimental MTLE models.
  • Synaptic reorganization of CA1 axons projecting to the subiculum increases inter-lamellar connectivity.
  • This reorganization provides a mechanism for translamellar synchronization of hyperexcitability.

Conclusions:

  • CA1 pyramidal axon plasticity is a significant, previously under-investigated mechanism in MTLE.
  • This plasticity contributes to pharmacologically intractable seizures by synchronizing hyperexcitability across hippocampal lamellae.

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