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Related Experiment Video

Updated: Dec 2, 2025

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Published on: August 17, 2021

Gene expression in the epileptic (EL) mouse hippocampus.

Tih-Shih Lee¹, Alexander Y Li², Amedeo Rapuano²

¹Department of Psychiatry, Duke University, North Carolina, United States of America.

Neurobiology of Disease

|November 6, 2020

Summary

This study explores molecular changes in the epileptic mouse hippocampus, revealing neuroprotective heat shock proteins and genes linked to hyperexcitability. Findings suggest activated glia contribute to epilepsy mechanisms.

Keywords:

Astrocytes Epileptic (EL) mouse Gene expression Immune mechanisms Microglia Neuroprotection Seizures

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Published on: August 15, 2017

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

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Last Updated: Dec 2, 2025

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Published on: August 17, 2021

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Temporal lobe epilepsy (TLE) involves neuronal loss and glial activation.
The epileptic (EL) mouse model lacks neuronal loss but shows glial proliferation, offering a unique study system.
Understanding molecular changes in the EL mouse hippocampus is crucial for elucidating the role of glia in epileptogenesis.

Purpose of the Study:

To identify molecular changes in the EL mouse hippocampus using high-throughput gene expression analysis.
To investigate the role of activated neuroglia in epilepsy pathogenesis in the absence of significant neuronal loss.

Main Methods:

High-throughput gene expression analysis of the hippocampus in the EL mouse model.
Comparative analysis of gene expression patterns associated with neuroprotection and hyperexcitability.

Main Results:

Upregulation of heat shock proteins (HSP70, HSP72, FOSL2, BAG3, DNAJB5) and downregulation of MALAT1 suggest neuroprotection.
Increased BDNF and immediate early gene expression, alongside downregulated GABRD, DBP, and MALAT1, indicate neuronal hyperexcitability.
Activated astrocytes show reduced glutamine synthetase, impairing glutamate clearance.
Activated microglia may mediate synaptic pruning via trogocytosis, reducing inhibition.

Conclusions:

Molecular changes in the EL mouse hippocampus involve both neuroprotective and hyperexcitability-associated gene expression.
Activated astrocytes and microglia contribute to hyperexcitability through impaired glutamate clearance and synaptic modification, respectively.
The EL mouse model provides valuable insights into glial roles in epileptogenesis.