What is GAERS?
GAERS (Genetic Absence Epilepsy Rats from Strasbourg) is a well-established genetic model for studying absence epilepsy, a type of generalized epilepsy characterized by brief, sudden lapses of consciousness.
Key Characteristics
- Spontaneous Seizures: GAERS rats spontaneously develop absence seizures starting around postnatal day 30 (P30)
- Spike-and-Wave Discharges (SWDs): Characteristic 7-11 Hz oscillations on EEG
- Genetic Model: Inherited trait, not induced by chemicals or lesions
- Human Relevance: Resembles childhood absence epilepsy in humans
- Thalamocortical Dysfunction: Circuit abnormalities in thalamus and cortex
Clinical Relevance
Absence epilepsy affects ~10-15% of children with epilepsy. GAERS provides a valuable model to study:
- Molecular mechanisms of seizure generation
- Developmental trajectory of epileptogenesis
- Potential therapeutic targets
- Circuit-level dysregulation
Why Study GAERS?
Unlike induced models, GAERS develops seizures naturally, making it ideal for studying the epileptogenic process - the transition from a normal to a seizure-prone brain.
Research Project
Spatiotemporal Transcriptomic Analysis of Epileptogenesis
This research project uses cutting-edge transcriptomic technologies to map gene expression changes during the critical window when GAERS rats transition from seizure-free to seizure-prone states.
Project Goals
- Identify molecular signatures of epileptogenesis by comparing pre-seizure (P15) and seizure-onset (P30) stages
- Map spatial gene expression patterns across brain regions using 10X Genomics Visium
- Discover potential therapeutic targets through pathway enrichment analysis
- Understand circuit-level dysregulation at the molecular level
Funding & Support
TÜBİTAK Project 122S431
This research is funded by The Scientific and Technological Research Council of Turkey (TÜBİTAK).
Principal Investigator:
Özkan Özdemir, Ph.D.
Experimental Approach
10X Genomics Spatial Transcriptomics
Visium spatial gene expression platform captures transcriptome-wide data while preserving tissue architecture.
- Technology: 10X Genomics Visium
- Samples: 8 (4 P15, 4 P30)
- Resolution: 55 μm spots, ~10 cells/spot
- DEGs: 1,079 per comparison
LCM/Bulk RNA-seq
Laser capture microdissection with bulk RNA-seq provides high-sensitivity gene expression profiling.
- Technology: LCM + Takara SMARTer kit
- Samples: 7 (2 Ga15, 5 Ga30)
- Platform: Illumina sequencing
- DEGs: 593 significant genes
Key Research Findings
Major Discoveries
Developmental Changes
Extensive transcriptional remodeling occurs during the P15-P30 window, with 593 DEGs (94% upregulated) in bulk RNA-seq and over 1,000 DEGs in spatial analysis.
Synaptic Dysregulation
Strong enrichment in postsynaptic density organization, synaptic plasticity, and maintenance of synaptic structures indicates circuit-level abnormalities.
Calcium Signaling
Dysregulation of calcium homeostasis and ion channel genes, including T-type calcium channels critical for absence seizure generation.
Biological Significance
These findings provide molecular evidence for the circuit-level dysfunction underlying epileptogenesis in GAERS. The identification of specific genes and pathways offers potential therapeutic targets for preventing or modulating absence seizure development.
About gaers.bio
gaers.bio is a comprehensive data portal designed to share research findings from spatiotemporal transcriptomic analysis of the GAERS epilepsy model with the scientific community.
What You Can Do Here
- Explore Research Data: Interactive visualizations of differential expression results
- Search Genes: Query 3,611 genes across all datasets with advanced filtering
- View Enrichment: GO and Reactome pathway analysis results
- Download Data: Access complete datasets in CSV format
- Understand Methods: Detailed experimental and analysis protocols
- Cite This Work: Proper citation information and references
Data Availability
All data presented on this website is freely available for research purposes. We encourage the scientific community to explore, analyze, and build upon these findings.
Contact & Collaboration
Principal Investigator
Özkan Özdemir, Ph.D.
For questions about this research or potential collaborations, please reach out through official channels.
Funding Acknowledgment
This research is supported by:
TÜBİTAK (The Scientific and Technological Research Council of Turkey)
Project Number: 122S431