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Epilepsy and Seizures: Overview01:24

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Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...
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Related Experiment Video

Updated: Feb 28, 2026

Preparation of Acute Human Hippocampal Slices for Electrophysiological Recordings
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Deciphering epileptogenic and activity-dependent gene programs in the human brain.

Qianyu Lin1, Chris Kang1, Andre M Xavier1

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, 11740, USA.

Biorxiv : the Preprint Server for Biology
|February 27, 2026
PubMed
Summary
This summary is machine-generated.

Chronic neuronal hyperactivity in drug-resistant epilepsy (DRE) triggers specific gene programs in human neurons. Some gene changes reflect heightened activity, while others indicate neuronal vulnerability and inflammation in DRE.

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Area of Science:

  • Neuroscience
  • Genomics
  • Molecular Biology

Background:

  • Elevated neuronal activity is central to brain function and implicated in neurological disorders like drug-resistant epilepsy (DRE).
  • Understanding activity-induced transcriptional programs in the human brain is crucial but poorly understood.
  • Animal models show defined responses, but human cellular specificity and pathological relevance in DRE are unclear.

Purpose of the Study:

  • To investigate activity-dependent gene expression in the human brain in the context of DRE.
  • To identify cell-type-specific transcriptional programs induced by the epileptogenic microenvironment.
  • To differentiate conserved responses to heightened activity from disease-specific programs in DRE.

Main Methods:

  • Application of single-nucleus and spatial transcriptomics.
  • Analysis of human cortical tissue from individuals with DRE (epileptogenic, non-epileptogenic, and acutely stimulated).
  • Profiling of 26 distinct cell types to assess gene expression patterns.

Main Results:

  • Glutamatergic neurons in specific cortical layers show sensitivity to the epileptogenic microenvironment, upregulating immediate-early genes, synaptic remodeling, and cellular stress programs.
  • About one-third of epilepsy-associated gene expression changes are also induced by acute neuronal stimulation, suggesting conserved activity responses.
  • Neurons in epileptogenic cortex may exhibit impaired metabolic adaptation to sustained energetic demands, unlike those responding to acute stimulation.
  • Microglia and circulating monocytes show immune activation, indicating myeloid-driven inflammation extending beyond the brain in DRE.

Conclusions:

  • Human activity-dependent gene programs are illuminated, revealing cell-type-specific responses to neuronal hyperactivity.
  • Findings highlight neuronal vulnerability and inflammatory signatures in the epileptogenic microenvironment of DRE.
  • A portion of gene expression changes in DRE reflects conserved responses to neuronal activity, not solely disease-specific mechanisms.