ArticleAnnals of clinical and translational neurology2022
Benchmarking the proteomic profile of animal models of mesial temporal epilepsy.
Article in Annals of clinical and translational neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Neurotoxicity-Based Toxicometabolomics ofACS omega · 2025Article
- Article
- Time- and Region-Specific Selection of Reference Genes in the Rat Brain in the Lithium-Pilocarpine Model of Acquired Temporal Lobe Epilepsy.Biomedicines · 2024Article
- Emerging Molecular Targets for Anti-Epileptogenic and Epilepsy Modifying Drugs.International journal of molecular sciences · 2023Review
- Interactions between astrocytes and extracellular matrix structures contribute to neuroinflammation-associated epilepsy pathology.Frontiers in molecular medicine · 2023Review
- Gene expression profile suggests different mechanisms underlying sporadic and familial mesial temporal lobe epilepsy.Experimental biology and medicine (Maywood, N.J.) · 2022Article
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Authors and funding
21 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesWe compared the proteomic signatures of the hippocampal lesion induced in three different animal models of mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE+HS): the systemic pilocarpine model (PILO), the intracerebroventricular kainic acid model (KA), and the perforant pathway stimulation model (PPS).
methodsWe used shotgun proteomics to analyze the proteomes and find enriched biological pathways of the dorsal and ventral dentate gyrus (DG) isolated from the hippocampi of the three animal models. We also compared the proteomes obtained in the animal models to that from the DG of patients with pharmacoresistant MTLE+HS.
resultsWe found that each animal model presents specific profiles of proteomic changes. The PILO model showed responses predominantly related to neuronal excitatory imbalance. The KA model revealed alterations mainly in synaptic activity. The PPS model displayed abnormalities in metabolism and oxidative stress. We also identified common biological pathways enriched in all three models, such as inflammation and immune response, which were also observed in tissue from patients. However, none of the models could recapitulate the profile of molecular changes observed in tissue from patients. SIGNIFICANCE: Our results indicate that each model has its own set of biological responses leading to epilepsy. Thus, it seems that only using a combination of the three models may one replicate more closely the mechanisms underlying MTLE+HS as seen in patients.
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