ArticleInternational journal of molecular sciences2024
Morphological and Functional Alterations in the CA1 Pyramidal Neurons of the Rat Hippocampus in the Chronic Phase of the Lithium-Pilocarpine Model of Epilepsy.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cholinergic modulation of hippocampal CA1 pyramidal cell excitability in ArxExperimental neurology · 2026Article
- Decorin Attenuates Epileptogenesis and Modulates Hippocampal Synaptic Plasticity via the mTOR Signalling Pathway.Neurochemical research · 2026Article
- Prefrontal Cortex 5-HT1A Receptor-Coupled Inwardly Rectifying Potassium Channels Decreased Seizure Susceptibility in Rat Models With Autism Spectrum Disorder.Neural plasticity · 2026Article
- Sleep and circadian rhythm disruptions in animal models of temporal lobe epilepsy.Frontiers in neuroscience · 2026Review
- Kainic acid status epilepticus - induced changes in the hippocampus and hypothalamus alter the effects of exogenous Orexin-A in the hippocampus.IBRO neuroscience reports · 2025Article
- Special Issue "Molecular and Cellular Mechanisms of Epilepsy-3rd Edition": Emerging Frontiers in Neuroinflammation, Network Remodeling, and Therapy.International journal of molecular sciences · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Epilepsy is known to cause alterations in neural networks. However, many details of these changes remain poorly understood. The objective of this study was to investigate changes in the properties of hippocampal CA1 pyramidal neurons and their synaptic inputs in a rat lithium-pilocarpine model of epilepsy. In the chronic phase of the model, we found a marked loss of pyramidal neurons in the CA1 area. However, the membrane properties of the neurons remained essentially unaltered. The results of the electrophysiological and morphological studies indicate that the direct pathway from the entorhinal cortex to CA1 neurons is reinforced in epileptic animals, whereas the inputs to them from CA3 are either unaltered or even diminished. In particular, the dendritic spine density in the
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Registered trials
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